Research activity information

• High-Fat Diet-Fed Kcnq1 Mutant Mice Have Reduced Pancreatic β-Cell Mass via Gene-Environment Interaction.

  Shun-Ichiro Asahara, Hiroyuki Inoue, Yuka Ihara, Kyoko Teruyama, Asuka Imai, Chisako Hara, Mizuki Hara, Masako Seike, Aisha Yokoi, Nozomi Kido, Hirotaka Suzuki, Ayumi Kanno, Yuka Inaba, Hitoshi Watanabe, Go Shioi, Maki Kimura-Koyanagi, Michihiro Matsumoto, Hiroshi Inoue, Keiichi I Nakayama, Wataru Ogawa, Masato Kasuga, Yoshiaki Kido

  BACKGROUND: The potassium voltage-gated channel subfamily Q member 1 (KCNQ1) gene has recently received much attention as a candidate susceptibility gene for type 2 diabetes mellitus, especially in Asian populations. We previously reported that Kcnq1 mutant mice exhibit reduced insulin secretion and hyperglycemia due to a decrease in pancreatic β-cell mass. Through in vivo and in vitro analyses, we ascertained that this mechanism is the result of the downregulation of the non-coding RNA 'Kcnq1ot1,' which is expressed in the paternal allele of the Kcnq1 gene region, causing an increase in the expression of the cell cycle inhibitor cyclin dependent kinase inhibitor 1C (Cdkn1c). It was found that decreased Kcnq1ot1 expression resulted in pancreatic β-cell failure; however, the degree of pancreatic β-cell volume reduction was not severe. METHODS: We induced obesity in Kcnq1ot1 truncation mice by feeding them a high-fat diet and evaluated pancreatic β-cell mass. RESULTS: In the present study, we reveal that CCAAT/enhancer binding protein beta (C/EBPβ), which is expressed at higher levels in pancreatic β-cells in obese individuals, further increases the expression of Cdkn1c, which is upregulated by the Kcnq1 gene mutation. We found that simultaneous Cdkn1c hypomethylation and C/EBPβ overexpression in pancreatic β-cells causes a synergistic decrease in pancreatic β-cell mass. CONCLUSION: This finding suggests that the synergistic effect of genetic factors such as Kcnq1 gene mutations and environmental factors such as obesity and overeating, which lead to increased expression of C/EBPβ, contribute to the regulation of pancreatic β-cell mass. This study is the first to show that the Kcnq1 gene is related to pancreatic β-cell mass through genetic-environment interactions.

  Jul. 2025, Diabetes & metabolism journal, English, International magazine

  Scientific journal


• miR378a-3p in serum extracellular vesicles is associated with pancreatic beta-cell mass in diabetic states.

  Aisha Yokoi, Shun-Ichiro Asahara, Hiroyuki Inoue, Ayano Goto, Masako Seike, Nozomi Kido, Hirotaka Suzuki, Ayumi Kanno, Maki Kimura-Koyanagi, Kenichi Uto, Jun Saegusa, Yoshiaki Kido, Wataru Ogawa

  The condition in which the insulin secretory ability of pancreatic β-cells decreases in diabetes is extremely important, but there are currently no biomarkers that reflect pancreatic β-cell failure. Therefore, we conducted a search for biomarkers, using pancreatic β-cell-specific 3-Phosphoinositide-dependent protein kinase 1 (PDK1) knockout mice, which develop severe hyperglycemia due to a decrease in pancreatic β-cell mass without insulin resistance. The analysis was performed in young mice when metabolic abnormalities were not yet apparent. Comprehensive analysis of microRNAs contained in extracellular vesicles in the blood of these mice revealed that miR378a-3p levels were significantly lower in PDK1 knockout mice than in control mice. Furthermore, in other mouse models of diabetes, namely, db/db mice and streptozotocin-induced diabetic mice, there was an increase and decrease in miR378a-3p expression, respectively, in line with the number of β-cells. These results suggest that miR378a-3p contained in serum extracellular vesicles is a biomarker that reflects pancreatic β-cell mass before the onset of diabetes. It is hoped that miR378a-3p can be utilized to realize earlier diagnosis and treatment of diabetes.

  Mar. 2025, Biochemical and biophysical research communications, 750, 151367 - 151367, English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• The usefulness of HbA1c measurement in diabetic mouse models using various devices.

  Kohya Miyazaki, Aisha Yokoi, Hiroyuki Inoue, Hirotaka Suzuki, Nozomi Kido, Ayumi Kanno, Maki Kimura-Koyanagi, Yoshiaki Kido, Shun-Ichiro Asahara

  In most cases, the diagnosis of diabetes in animal models is based solely on blood glucose levels. While hemoglobin A1c (HbA1c) is widely used in the diagnosis of diabetes in humans, it is rarely measured in mice in diabetes research. This is thought to be because there are no established reference values for mouse HbA1c, as well as the fact that there are very few reports on the variability and reproducibility of measurements taken using different devices. In this study, we measured HbA1c levels in diabetic mouse models using different devices based on different principles, including capillary electrophoresis, high-performance liquid chromatography, and enzymatic methods, and compared the results. A positive correlation was observed between blood glucose and HbA1c levels in all measurement methods, and high reproducibility was confirmed in the measurement of HbA1c. However, HbA1c levels measured using the enzymatic method were slightly higher than those measured using the other two methods. In addition, an examination of diabetic mice given a sodium-glucose cotransporter 2 inhibitor, which is used to treat diabetes, revealed that there was a 2-week difference in the fluctuation of mouse HbA1c levels compared with the fluctuation of blood glucose levels. Based on these results, it is thought that HbA1c can be a reliable indicator in diabetic mouse models, and it is expected to make the evaluation of abnormal glucose metabolism in mice more reliable.

  Jan. 2025, Experimental animals, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Protective effect of CK2 against endoplasmic reticulum stress in pancreatic β cells

  Tomoko Takai, Shun-ichiro Asahara, Hiroko Ikushiro, Kenta Kobayashi, Takato Yano, Yoshiaki Kido, Wataru Ogawa

  Springer Science and Business Media LLC, Nov. 2024, Diabetology International, 16(1) (1), 131 - 144

  Scientific journal


• Dapagliflozin administration to a mouse model of type 2 diabetes induces DNA methylation and gene expression changes in pancreatic islets.

  Aisha Yokoi, Shun-Ichiro Asahara, Hiroyuki Inoue, Masako Seike, Nozomi Kido, Hirotaka Suzuki, Ayumi Kanno, Maki Kimura-Koyanagi, Yoshiaki Kido, Wataru Ogawa

  Decreased pancreatic β-cell volume is a serious problem in patients with type 2 diabetes mellitus, and there is a need to establish appropriate treatments. Increasingly, sodium/glucose cotransporter 2 (SGLT2) inhibitors, which have a protective effect on pancreatic β-cells, are being prescribed to treat diabetes; however, the underlying mechanism is not well understood. We previously administered SGLT2 inhibitor dapagliflozin to a mouse model of type 2 diabetes and found significant changes in gene expression in the early-treated group, which led us to hypothesize that epigenetic regulation was a possible mechanism of these changes. Therefore, we performed comprehensive DNA methylation analysis by methylated DNA immunoprecipitation using isolated pancreatic islets after dapagliflozin administration to diabetic model mice. As a result, we identified 31 genes with changes in expression due to DNA methylation changes. Upon immunostaining, cystic fibrosis transmembrane conductance regulator and cadherin 24 were found to be upregulated in islets in the dapagliflozin-treated group. These molecules may contribute to the maintenance of islet morphology and insulin secretory capacity, suggesting that SGLT2 inhibitors' protective effect on pancreatic β-cells is accompanied by DNA methylation changes, and that the effect is long-term and not temporary. In future diabetes care, SGLT2 inhibitors may be expected to have positive therapeutic effects, including pancreatic β-cell protection.

  Sep. 2024, Biochemical and biophysical research communications, 725, 150254 - 150254, English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• A High Fibrosis-4 Index is Associated with a Reduction in the Estimated Glomerular Filtration Rate in Non-obese Japanese Patients with Type 2 Diabetes Mellitus.

  Hiroyuki Inoue, Shun-Ichiro Asahara, Fumihiko Nakamura, Yoshiaki Kido

  Liver fibrosis is associated with non-alcoholic fatty liver disease (NAFLD), and one of the most important risk factors for NAFLD is type 2 diabetes (T2DM). The Fibrosis-4 (FIB-4) index, a noninvasive liver fibrosis score, has been found to be useful for estimating liver fibrosis. Because individuals with non-obese NAFLD were recently reported to be metabolically unhealthy and have a higher risk of T2DM than individuals with obese NAFLD, we hypothesized that the clinical factors related to a high FIB-4 index would differ between non-obese and obese Japanese T2DM patients. Accordingly, we examined the relationship between clinical factors and the FIB-4 index in non-obese and obese Japanese patients with T2DM. We divided 265 patients into two groups by BMI level - a non-obese group (n = 149) and an obese group (n = 116) - and examined the correlation between the FIB-4 index and clinical parameters. Single regression analysis revealed that a high FIB-4 index was correlated with a reduction in the estimated glomerular filtration rate and hypertension in the non-obese group. Importantly, multiple regression analysis showed that only a reduction in the estimated glomerular filtration rate was significantly associated with a high FIB-4 index in the non-obese group. These results demonstrated that non-obese T2DM patients with a high FIB-4 index might be at risk of kidney dysfunction. Our findings may enable the more appropriate treatment of T2DM patients based on BMI level.

  Apr. 2024, The Kobe journal of medical sciences, 70(1) (1), E39-E45, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• 膵β細胞におけるmTORC1活性化が膵島可塑性に及ぼす影響の検討

  木戸 希, 淺原 俊一郎, 清家 雅子, 木村 真希, 鈴木 宏隆, 横井 愛紗, 椎木 幾久子, 田部 勝也, 木戸 良明, 小川 渉

  (一社)日本糖尿病学会, Apr. 2024, 糖尿病, 67(Suppl.1) (Suppl.1), S - 160, Japanese


• Dietary Intervention for Control of Clinical Symptom in Patients with Systemic Metal Allergy: A Single Center Randomized Controlled Clinical Study.

  Reiko Mikajiri, Atsushi Fukunaga, Makoto Miyoshi, Noriaki Maeshige, Ken Washio, Taro Masaki, Chikako Nishigori, Ikuko Yamamoto, Akiyo Toda, Michiko Takahashi, Shun-Ichiro Asahara, Yoshiaki Kido, Makoto Usami

  Patients with eczema with a systemic metal allergy, such as nickel (Ni), cobalt (Co), chromium (Cr), and tin (Sn), should pay attention to symptomatic exacerbation by excessive metal intake in food. However, dietary intervention for systemic metal allergy can be difficult. In this study, we evaluated the effect of dietary intervention by a registered dietitian on clinical symptoms in patients with a systemic metal allergy. Forty-four patients with cutaneous symptoms who were diagnosed with a metal allergy were randomly assigned to the dietary intervention group (DI group, n = 29) by a registered dietitian or the control group (C group, n = 15). The DI group was individually instructed by a registered dietitian how to implement a metal-restricted diet and then evaluated 1 month later. Dermatologists treated skin lesions of patients in both groups. Skin symptoms assessed by the Severity Scoring of Atopic Dermatitis (SCORAD) index, blood tests, and urinary metal excretion were evaluated. The DI group showed decreased Ni, Co, Cr, and Sn intake (all P ≤ 0.05), and an improved total SCORAD score, eczema area, erythema, edema/papulation, oozing/crust, excoriation, lichenization and dryness after 1 month of intervention compared with before the intervention (all P ≤ 0.05). However, the C group showed decreased Ni and Sn intake and an improved oozing/crust score (all P < 0.05). It showed the effective reduction of dietary metal intake controls dermatitis due to a metal allergy. In conclusion, dietary intervention by a registered dietitian is effective in improving skin symptoms with a reduction in metal intake.

  Jan. 2024, The Kobe journal of medical sciences, 69(4) (4), E129-E143, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Hepatic FASN deficiency differentially affects nonalcoholic fatty liver disease and diabetes in mouse obesity models.

  Toshiya Matsukawa, Takashi Yagi, Tohru Uchida, Mashito Sakai, Masaru Mitsushima, Takao Naganuma, Hiroyuki Yano, Yuka Inaba, Hiroshi Inoue, Keisuke Yanagida, Masaaki Uematsu, Kazuki Nakao, Harumi Nakao, Atsu Aiba, Yoji Nagashima, Tetsuya Kubota, Naoto Kubota, Yoshihiko Izumida, Naoya Yahagi, Hiroyuki Unoki-Kubota, Yasushi Kaburagi, Shun-Ichiro Asahara, Yoshiaki Kido, Hideo Shindou, Michiko Itoh, Yoshihiro Ogawa, Shiro Minami, Yasuo Terauchi, Kazuyuki Tobe, Kohjiro Ueki, Masato Kasuga, Michihiro Matsumoto

  Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes are interacting comorbidities of obesity, and increased hepatic de novo lipogenesis (DNL), driven by hyperinsulinemia and carbohydrate overload, contributes to their pathogenesis. Fatty acid synthase (FASN), a key enzyme of hepatic DNL, is upregulated in association with insulin resistance. However, the therapeutic potential of targeting FASN in hepatocytes for obesity-associated metabolic diseases is unknown. Here, we show that hepatic FASN deficiency differentially affects NAFLD and diabetes depending on the etiology of obesity. Hepatocyte-specific ablation of FASN ameliorated NAFLD and diabetes in melanocortin 4 receptor-deficient mice but not in mice with diet-induced obesity. In leptin-deficient mice, FASN ablation alleviated hepatic steatosis and improved glucose tolerance but exacerbated fed hyperglycemia and liver dysfunction. The beneficial effects of hepatic FASN deficiency on NAFLD and glucose metabolism were associated with suppression of DNL and attenuation of gluconeogenesis and fatty acid oxidation, respectively. The exacerbation of fed hyperglycemia by FASN ablation in leptin-deficient mice appeared attributable to impairment of hepatic glucose uptake triggered by glycogen accumulation and citrate-mediated inhibition of glycolysis. Further investigation of the therapeutic potential of hepatic FASN inhibition for NAFLD and diabetes in humans should thus consider the etiology of obesity.

  Sep. 2023, JCI insight, 8(17) (17), English, International magazine

  Scientific journal


• 膵β細胞におけるmTORC1活性化は膵外分泌細胞への分化を誘導する

  清家 雅子, 淺原 俊一郎, 木村 真希, 鈴木 宏隆, 横井 愛紗, 椎木 幾久子, 田部 勝也, 木戸 良明, 小川 渉

  (一社)日本糖尿病学会, Apr. 2023, 糖尿病, 66(Suppl.1) (Suppl.1), S - 186, Japanese


• 膵β細胞におけるmTORC1活性化は膵外分泌細胞への分化を誘導する

  清家 雅子, 淺原 俊一郎, 木村 真希, 鈴木 宏隆, 横井 愛紗, 椎木 幾久子, 田部 勝也, 木戸 良明, 小川 渉

  (一社)日本糖尿病学会, Apr. 2023, 糖尿病, 66(Suppl.1) (Suppl.1), S - 186, Japanese


• Chlorogenic Acid and Caffeine in Coffee Restore Insulin Signaling in Pancreatic Beta Cells.

  Yuka Ihara, Shun-Ichiro Asahara, Hiroyuki Inoue, Masako Seike, Misaki Ando, Hiroki Kabutoya, Maki Kimura-Koyanagi, Yoshiaki Kido

  The incidence of type 2 diabetes is reported to be lower in frequent coffee drinkers than in non-coffee drinkers. To elucidate the mechanism by which coffee prevents the onset of type 2 diabetes, we analyzed how caffeine and chlorogenic acid, which are components of coffee, alter insulin signaling in MIN6 cells, a mouse pancreatic Β cell line. The results showed that caffeine improved insulin signaling under endoplasmic reticulum stress, and chlorogenic acid protected pancreatic Β cells by enhancing the expression of insulin receptor substrate 2 via cAMP response element-binding protein and promoting insulin signaling downstream of insulin receptor substrate 2. In addition, chlorogenic acid was a potent antioxidant for the protection of pancreatic Β cells. Furthermore, in vivo and in vitro analyses revealed that the pancreatic Β cell-protective effect of chlorogenic acid was mediated by the alleviation of endoplasmic reticulum stress. The results suggest that these components of coffee have the potential to reduce the pathogenesis of type 2 diabetes and improve pancreatic Β cell insufficiency.

  Mar. 2023, The Kobe journal of medical sciences, 69(1) (1), E1-E8, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• l-Asparaginase regulates mTORC1 activity via a TSC2-dependent pathway in pancreatic beta cells.

  Masako Seike, Shun-Ichiro Asahara, Hiroyuki Inoue, Michiyo Kudo, Ayumi Kanno, Aisha Yokoi, Hirotaka Suzuki, Maki Kimura-Koyanagi, Yoshiaki Kido, Wataru Ogawa

  Eif2ak4, a susceptibility gene for type 2 diabetes, encodes GCN2, a molecule activated by amino acid deficiency. Mutations or deletions in GCN2 in pancreatic β-cells increase mTORC1 activity by decreasing Sestrin2 expression in a TSC2-independent manner. In this study, we searched for molecules downstream of GCN2 that suppress mTORC1 activity in a TSC2-dependent manner. To do so, we used a pull-down assay to identify molecules that competitively inhibit the binding of the T1462 phosphorylation site of TSC2 to 14-3-3. l-asparaginase was identified. Although l-asparaginase is frequently used as an anticancer drug for acute lymphoblastic leukemia, little is known about endogenous l-asparaginase. l-Asparaginase, which is expressed downstream of GCN2, was found to bind 14-3-3 and thereby to inhibit its binding to the T1462 phosphorylation site of TSC2 and contribute to TSC2 activation and mTORC1 inactivation upon TSC2 dephosphorylation. Further investigation of the regulation of mTORC1 activity in pancreatic β-cells by l-asparaginase should help to elucidate the mechanism of diabetes and insulin secretion failure during anticancer drug use.

  Feb. 2023, Biochemical and biophysical research communications, 652, 121 - 130, English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Roles of mTOR in the Regulation of Pancreatic β-Cell Mass and Insulin Secretion.

  Shun-Ichiro Asahara, Hiroyuki Inoue, Hitoshi Watanabe, Yoshiaki Kido

  Pancreatic β-cells are the only type of cells that can control glycemic levels via insulin secretion. Thus, to explore the mechanisms underlying pancreatic β-cell failure, many reports have clarified the roles of important molecules, such as the mechanistic target of rapamycin (mTOR), which is a central regulator of metabolic and nutrient cues. Studies have uncovered the roles of mTOR in the function of β-cells and the progression of diabetes, and they suggest that mTOR has both positive and negative effects on pancreatic β-cells in the development of diabetes.

  Apr. 2022, Biomolecules, 12(5) (5), English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• 膵β細胞におけるmTORC1恒常的活性化と膵島可塑性の関連についての検討

  清家 雅子, 淺原 俊一郎, 伊東 春香, 木村 真希, 鈴木 宏隆, 横井 愛紗, 神野 歩, 木戸 良明, 小川 渉

  (一社)日本糖尿病学会, Apr. 2022, 糖尿病, 65(Suppl.1) (Suppl.1), S - 217, Japanese


• COVID-19治療におけるCasirivimab-Imdevimab投与後の抗SARS-CoV-2抗体価推移と臨床経過 抗体カクテル療法における抗SARS-CoV-2抗体価測定の意義

  井上 裕行, 中山 奈月, 高谷 美結, 仲北 友子, 木戸 良明, 佐藤 公俊, 前田 光一, 中村 文彦

  (一社)日本臨床衛生検査技師会, Apr. 2022, 医学検査, 71(2) (2), 257 - 262, Japanese


• Regulation of Pancreatic β-Cell Mass by Gene-Environment Interaction.

  Shun-Ichiro Asahara, Hiroyuki Inoue, Yoshiaki Kido

  The main pathogenic mechanism of diabetes consists of an increase in insulin resistance and a decrease in insulin secretion from pancreatic β-cells. The number of diabetic patients has been increasing dramatically worldwide, especially in Asian people whose capacity for insulin secretion is inherently lower than that of other ethnic populations. Causally, changes of environmental factors in addition to intrinsic genetic factors have been considered to have an influence on the increased prevalence of diabetes. Particular focus has been placed on "gene-environment interactions" in the development of a reduced pancreatic β-cell mass, as well as type 1 and type 2 diabetes mellitus. Changes in the intrauterine environment, such as intrauterine growth restriction, contribute to alterations of gene expression in pancreatic β-cells, ultimately resulting in the development of pancreatic β-cell failure and diabetes. As a molecular mechanism underlying the effect of the intrauterine environment, epigenetic modifications have been widely investigated. The association of diabetes susceptibility genes or dietary habits with gene-environment interactions has been reported. In this review, we provide an overview of the role of gene-environment interactions in pancreatic β-cell failure as revealed by previous reports and data from experiments.

  Jan. 2022, Diabetes & metabolism journal, 46(1) (1), 38 - 48, English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Oral administration of D-serine prevents the onset and progression of colitis in mice.

  Takehito Asakawa, Michio Onizawa, Chikako Saito, Rie Hikichi, Daiki Yamada, Ai Minamidate, Tomoaki Mochimaru, Shun-Ichiro Asahara, Yoshiaki Kido, Shigeru Oshima, Takashi Nagaishi, Kiichiro Tsuchiya, Hiromasa Ohira, Ryuichi Okamoto, Mamoru Watanabe

  BACKGROUND: L-amino acids are the predominant forms of organic molecules on the planet, but recent studies have revealed that various foods contain D-amino acids, the enantiomers of L-amino acids. Though diet plays important roles in both the development and progression of inflammatory bowel disease (IBD), to our best knowledge, there has been no report on any potential interactions between D-amino acids and IBD. In this report, we aim to assess the effects of D-serine in a murine model of IBD. MATERIALS AND METHODS: To induce chronic colitis, naïve CD4 T cells (CD4+ CD62+ CD44low) from wild-type mice were adoptively transferred into Rag2-/- mice, after or before the mice were orally administered with D-serine. In vitro proliferation assays were performed to assess naïve CD4 T cell activation under the Th-skewing conditions in the presence of D-serine. RESULTS: Mice treated with D-serine prior to the induction of colitis exhibited a reduction in T-cell infiltration into the lamina propria and colonic inflammation that were not seen in mice fed with water alone or L-serine. Moreover, D-serine suppressed the progression of chronic colitis when administered after the disease induction. Under in vitro conditions, D-serine suppressed the proliferation of activated CD4 T cells and limited their ability to differentiate to Th1 and Th17 cells. CONCLUSION: Our results suggest that D-serine not only can prevent, but also has efficacious effects as a treatment for IBD.

  Aug. 2021, Journal of gastroenterology, 56(8) (8), 732 - 745, English, Domestic magazine

  Scientific journal


• Glutamate is an essential mediator in glutamine-amplified insulin secretion.

  Guirong Han, Harumi Takahashi, Naoya Murao, Ghupurjan Gheni, Norihide Yokoi, Yoshiyuki Hamamoto, Shun-Ichiro Asahara, Yutaka Seino, Yoshiaki Kido, Susumu Seino

  AIMS/INTRODUCTION: Glutamine is the most abundant amino acid in the circulation. In this study, we investigated cell signaling in the amplification of insulin secretion by glutamine. MATERIALS AND METHODS: Clonal pancreatic β-cells MIN6-K8, wild-type B6 mouse islets, glutamate dehydrogenase (GDH) knockout clonal β-cells (Glud1KOβCL), and glutamate-oxaloacetate transaminase 1 (GOT1) knockout clonal β-cells (Got1KOβCL) were studied. Insulin secretion from these cells and islets was examined under various conditions, and intracellular glutamine metabolism was assessed by metabolic flux analysis. Intracellular Ca2+ concentration ([Ca2+ ]i ) was also measured. RESULTS: Glutamine dose-dependently amplified insulin secretion in the presence of high glucose in both MIN6-K8 cells and Glud1KOβCL. Inhibition of glutaminases, the enzymes that convert glutamine to glutamate, dramatically reduced the glutamine-amplifying effect on insulin secretion. A substantial amount of glutamate was produced from glutamine through direct conversion by glutaminases. Glutamine also increased [Ca2+ ]i at high glucose, which was abolished by inhibition of glutaminases. Glutamic acid dimethylester (dm-Glu), a membrane permeable glutamate precursor that is converted to glutamate in cells, increased [Ca2+ ]i as well as induced insulin secretion at high glucose. These effects of glutamine and dm-Glu were dependent on calcium influx. Glutamine also induced insulin secretion in clonal β-cells MIN6-m14, which otherwise exhibit no insulin secretory response to glucose. CONCLUSIONS: Glutamate converted from glutamine is an essential mediator that enhances calcium signaling in the glutamine-amplifying effect on insulin secretion. Our data also suggest that glutamine exerts a permissive effect on glucose-induced insulin secretion.

  Jan. 2021, Journal of diabetes investigation, 12(6) (6), 920 - 930, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Effect of a Combined Exercise and Cognitive Activity Intervention on Cognitive Function in Community-dwelling Older Adults: A Pilot Randomized Controlled Trial.

  Shunsuke Murata, Rei Ono, Hisafumi Yasuda, Rumi Tanemura, Yoshiaki Kido, Hisatomo Kowa

  OBJECTIVE: The purpose of this study is to investigate the effect of an intervention combining exercise and cognitive activity on cognitive function in healthy older adults. METHODS: This pilot randomized controlled trial recruited 33 eligible, healthy communitydwelling older adults (mean age, 77.1 years old; women, 51.5%), who were divided into intervention and waitlist control groups. The intervention group was engaged weekly in a group activity comprising exercise and discussions of homework, which included reading aloud, simple arithmetic, and simple activities, like spotting differences, for cognitive stimulation. They were also required to complete cognitive activity homework twice a week. The waitlist control group received no intervention. The main outcomes were cognitive function assessed using the Mini-Mental State Examination, delayed recall score on the Logical Memory IIA of the Wechsler Memory Scale Revised, Trail Making Test, and digit symbol substitution test. RESULTS: According to the results, Mini-Mental State Examination scores were maintained in the intervention group but declined in the control group [Mean change in outcomes in control group (95% confidence interval): -1.68 (-2.89 to -0.48)]. Additional mean change in outcomes in intervention group were found [1.68 (0.02 to 3.35)]. CONCLUSIONS: Interventions combining exercise and cognitive activity can be helpful for preserving cognitive function in healthy older adults.

  2021, Physical therapy research, 24(2) (2), 112 - 119, English, Domestic magazine

  [Refereed]

  Scientific journal


• Histone deacetylase 6 regulates insulin signaling in pancreatic β cells

  Hiroyuki Inoue, Shun-ichiro Asahara, Yumiko Sugiura, Yukina Kawada, Asuka Imai, Chisako Hara, Ayumi Kanno, Maki Kimura-Koyanagi, Yoshiaki Kido

  Elsevier BV, Nov. 2020, Biochemical and Biophysical Research Communications

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• グルタミンによるインスリン分泌増強機構の解明

  韓 桂栄, 高橋 晴美, 村尾 直哉, ゲニ・グブルジャン, 太田 新菜, 浜本 芳之, 清野 裕, 横井 伯英, 木戸 良明, 清野 進

  (一社)日本糖尿病学会, Aug. 2020, 糖尿病, 63(Suppl.1) (Suppl.1), S - 195, Japanese


• 地域在住高齢がんサバイバーにおける運動機能と精神機能、生化学データの特徴

  小野 玲, 牧浦 大祐, 内田 一彰, 河原田 里果, 木戸 良明, 安田 尚史, 古和 久朋

  (NPO)日本緩和医療学会, Aug. 2020, Palliative Care Research, 15(Suppl.) (Suppl.), S241 - S241, Japanese


• 地域在住高齢者における自己記入によるDASC-21の特性

  小野 玲, 内田 一彰, 河原田 里果, 木戸 良明, 安田 尚史, 古和 久朋

  (一社)日本老年医学会, Jul. 2020, 日本老年医学会雑誌, 57(Suppl.) (Suppl.), 81 - 81, Japanese


• 地域在住高齢者における自己記入によるDASC-21の特性

  小野 玲, 内田 一彰, 河原田 里果, 木戸 良明, 安田 尚史, 古和 久朋

  (一社)日本老年医学会, Jul. 2020, 日本老年医学会雑誌, 57(Suppl.) (Suppl.), 81 - 81, Japanese


• GCN2 regulates pancreatic β cell mass by sensing intracellular amino acid levels.

  Ayumi Kanno, Shun-Ichiro Asahara, Ayuko Furubayashi, Katsuhisa Masuda, Risa Yoshitomi, Emi Suzuki, Tomoko Takai, Maki Kimura-Koyanagi, Tomokazu Matsuda, Alberto Bartolome, Yushi Hirota, Norihide Yokoi, Yuka Inaba, Hiroshi Inoue, Michihiro Matsumoto, Kenichi Inoue, Takaya Abe, Fan-Yan Wei, Kazuhito Tomizawa, Wataru Ogawa, Susumu Seino, Masato Kasuga, Yoshiaki Kido

  EIF2AK4, which encodes the amino acid deficiency-sensing protein GCN2, has been implicated as a susceptibility gene for type 2 diabetes in the Japanese population. However, the mechanism by which GCN2 affects glucose homeostasis is unclear. Here, we show that insulin secretion is reduced in individuals harboring the risk allele of EIF2AK4 and that maintenance of GCN2-deficient mice on a high-fat diet results in a loss of pancreatic β cell mass. Our data suggest that GCN2 senses amino acid deficiency in β cells and limits signaling by mechanistic target of rapamycin complex 1 to prevent β cell failure during the consumption of a high-fat diet.

  May 2020, JCI insight, 5(9) (9), English, International magazine

  [Refereed]

  Scientific journal


• CK2活性化は膵β細胞において小胞体ストレスを改善する

  高井 智子, 松田 友和, 清家 雅子, 淺原 俊一郎, 木村 真希, 生城 浩子, 矢野 貴人, 小林 憲太, 小川 渉, 木戸 良明

  日本臨床分子医学会, Apr. 2020, 日本臨床分子医学会学術総会プログラム・抄録集, 57回, 76 - 76, Japanese


• En face slab optical coherence tomography imaging successfully monitors progressive degenerative changes in the innermost layer of the diabetic retina.

  Atsuko Katsuyama, Sentaro Kusuhara, Shun-Ichiro Asahara, Shun-Ichiro Nakai, Sotaro Mori, Wataru Matsumiya, Akiko Miki, Takuji Kurimoto, Hisanori Imai, Yoshiaki Kido, Wataru Ogawa, Makoto Nakamura

  OBJECTIVE: To evaluate the usefulness of en face slab optical coherence tomography (OCT) imaging for monitoring diabetic retinal neurodegeneration with supporting animal experimental data. RESEARCH DESIGN AND METHODS: We retrospectively examined 72 diabetic eyes over 3 years using Cirrus-HD OCT. Two-dimensional en face slab OCT images of the innermost retina were reconstructed and graded according to the ratio of dark area to total area, and relative red, green, and blue color area ratios were calculated and used as indexes for each en face slab OCT image. Values from en face OCT images were used for statistical analyses. To obtain insight into the pathogenesis of diabetic retinal neurodegeneration, we used the InsPr-Cre;Pdk1flox/flox diabetic mouse model. RESULTS: Both OCT grade and relative red color area ratio significantly increased with the advancing stage of diabetic retinopathy (p=0.018 and 0.006, respectively). After a mean follow-up period of 4.6 years, the trend was unchanged in the analyses of 42 untreated eyes (p<0.001 and 0.001, respectively). Visual acuity showed a weak but significant negative correlation with the red color ratio on en face slab OCT images, but central retinal thickness did not exhibit a clinically meaningful correlation with values obtained from en face slab OCT images. Immunohistochemical analyses of InsPr-Cre;Pdk1flox/flox diabetic mice demonstrated the loss of ganglion axon bundles and thinning of laminin without apparent retinal vascular change at the age of 20 weeks. CONCLUSIONS: En face slab OCT imaging would be a novel useful modality for the assessment of diabetic retinal neurodegeneration as it could detect subtle optical changes occurring in the innermost retina in diabetic eyes. Our animal experimental data suggest that dark areas observed on en face slab OCT images might be the impairment of the extracellular matrix as well as neurons.

  Mar. 2020, BMJ open diabetes research & care, 8(1) (1), English, International magazine

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• 金属アレルギー患者に対する管理栄養士による栄養食事指導の効果 ランダム化比較試験

  三ヶ尻 礼子, 福永 淳, 三好 真琴, 前重 伯壮, 鷲尾 健, 正木 太郎, 田渕 聡子, 脇田 久美子, 山西 美沙, 中谷 早希, 菅 里沙子, 齋藤 沙緒理, 河村 弘美, 山本 育子, 高橋 路子, 木戸 良明, 錦織 千佳子, 宇佐美 眞

  (一社)日本病態栄養学会, Jan. 2020, 日本病態栄養学会誌, 23(Suppl.) (Suppl.), S - 2, Japanese

  [Refereed]


• Association between mean platelet volume in the pathogenesis of type 2 diabetes mellitus and diabetic macrovascular complications in Japanese patients.

  Hiroyuki Inoue, Mayumi Saito, Kumiko Kouchi, Shun-Ichiro Asahara, Fumihiko Nakamura, Yoshiaki Kido

  AIMS/INTRODUCTION: Mean platelet volume (MPV) is a widely used biological marker of platelet function and activity. Increased MPV is associated with accelerated thrombopoiesis and an elevated risk of cardiovascular disease. However, it is not known whether higher MPV is related to the pathogenesis of type 2 diabetes and diabetic macrovascular complications in Japanese patients. Therefore, we analyzed MPV and its correlation with atherosclerosis in Japanese patients with type 2 diabetes and those who had prediabetes. MATERIALS AND METHODS: We divided the patients into three groups: normoglycemic patients (n = 56), prediabetes patients (n = 44) and type 2 diabetes patients group, (n = 115). We measured platelet parameters and evaluated arterial stiffness in the three groups. RESULTS: Significantly higher MPV was found in the type 2 diabetes mellitus and prediabetes patients compared with normoglycemic patients. MPV was significantly correlated with fasting blood glucose and glycated hemoglobin levels. Multiple linear regression analysis showed that MPV was positively correlated with HbA1c, even after adjustment for confounding factors. In the evaluation of arterial stiffness by measuring the cardio-ankle vascular index and maximum intima-media thickness, MPV showed a positive correlation with these parameters. CONCLUSIONS: These findings suggest that MPV was significantly increased in the early stage of type 2 diabetes. We showed positive correlations between MPV and HbA1c levels, and between MPV and arterial stiffness in Japanese patients with type 2 diabetes.

  Dec. 2019, Journal of diabetes investigation, English, Domestic magazine

  [Refereed]

  Link to Kobe Univ. Repository (Kernel)


• Early administration of dapagliflozin preserves pancreatic beta cell mass through a legacy effect in type 2 diabetic mice.

  Kanno A, Asahara S, Kawamura M, Suzuki E, Takai T, Kimura-Koyanagi M, Matsuda T, Okada Y, Ogawa W, KIDO YOSHIAKI

  May 2019, J. Diab. Invest., 10(3) (3), 577 - 590, English

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• 膵β細胞の小胞体ストレス誘導性アポトーシスにおけるCK2βの役割

  高井 智子, 松田 友和, 井上 佳歩, 淺原 俊一郎, 神野 歩, 木村 真希, 小川 渉, 木戸 良明

  日本臨床分子医学会, Apr. 2019, 日本臨床分子医学会学術総会プログラム・抄録集, 56回, 65 - 65, Japanese


• 膵β細胞特異的TSC2ノックアウトマウスにおける膵β細胞不全発症機序の解明

  伊東 春香, 淺原 俊一郎, 原 千佐子, 木村 真希, 神野 歩, 高井 智子, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2019, 糖尿病, 62(Suppl.1) (Suppl.1), S - 257, Japanese


• 2型糖尿病の病態把握におけるMPV(平均血小板容積)の有用性に関する検討

  井上 裕行, 斉藤 真裕美, 胡内 久美子, 淺原 俊一郎, 木戸 良明, 中村 文彦

  (一社)日本糖尿病学会, Apr. 2019, 糖尿病, 62(Suppl.1) (Suppl.1), S - 112, Japanese


• PHD3 regulates glucose metabolism by suppressing stress-induced signalling and optimising gluconeogenesis and insulin signalling in hepatocytes

  Yano Hiroyuki, Sakai Mashito, Matsukawa Toshiya, Yagi Takashi, Naganuma Takao, Mitsushima Masaru, Iida Satoshi, Inaba Yuka, Inoue Hiroshi, Unoki-Kubota Hiroyuki, Kaburagi Yasushi, Asahara Shun-ichiro, Kido Yoshiaki, Minami Shiro, Kasuga Masato, Matsumoto Michihiro

  Glucagon-mediated gene transcription in the liver is critical for maintaining glucose homeostasis. Promoting the induction of gluconeogenic genes and blocking that of insulin receptor substrate (Irs)2 in hepatocytes contributes to the pathogenesis of type 2 diabetes. However, the molecular mechanism by which glucagon signalling regulates hepatocyte metabolism is not fully under

  Springer Nature, Sep. 2018, Scientific Reports, (8) (8), English

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• 2型糖尿病感受性遺伝子GCN2はSestrin2を介して膵β細胞量の調節に関与する

  古林 鮎子, 神野 歩, 淺原 俊一郎, 松田 友和, 木村 真希, 木戸 良明

  (一社)日本内分泌学会, Apr. 2018, 日本内分泌学会雑誌, 94(1) (1), 323 - 323, Japanese


• 2型糖尿病に対する新規分子標的治療薬の確立

  松田 友和, 高井 智子, 鈴木 江美, 神野 歩, 木村 真希, 淺原 俊一郎, 小川 渉, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61(Suppl.1) (Suppl.1), S - 133, Japanese


• 膵β細胞の小胞体ストレス誘導性アポトーシスにおけるCK2βの役割

  高井 智子, 松田 友和, 井上 佳歩, 鈴木 江美, 木村 真希, 淺原 俊一郎, 小川 渉, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61(Suppl.1) (Suppl.1), S - 261, Japanese


• ヒトiPS細胞を用いた膵内分泌細胞への分化誘導

  山田 瑞姫, 淺原 俊一郎, 下野 名奈子, 原 瑞季, 松田 友和, 高井 智子, 鈴木 江美, 木村 真希, 神野 歩, 青井 貴之, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61(Suppl.1) (Suppl.1), S - 386, Japanese


• グルタミン-グルタミン酸シグナルによるインスリン分泌増強機構の解明

  韓 桂栄, 横井 伯英, グプルジャン・ゲニ, 村尾 直哉, 高橋 晴美, 清野 裕, 木戸 良明, 清野 進

  (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61(Suppl.1) (Suppl.1), S - 252, Japanese

  [Refereed]


• メトホルミン内服患者におけるビタミンB12欠乏の実態調査

  菅原 健二, 岡田 裕子, 野村 和弘, 山田 倫子, 中川 靖, 福岡 秀規, 廣田 勇士, 細岡 哲也, 坂口 一彦, 木戸 良明, 小川 渉

  (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61(Suppl.1) (Suppl.1), S - 238, Japanese

  [Refereed]


• BIA (bioelectrical impedance analysis) 法で定量した日本人糖尿病患者の体組成と栄養評価法の検討

  松尾真里, USAMI MAKOTO, MIYOSHI MAKOTO, 上野真波, 梶田歩, 山下勇人, 植村弥希子, 井上岳人, 内田絢子, 芝唯, 三ヶ尻礼子, 山本育子, 戸田明代, TAKAHASHI MICHIKO, KIDO YOSHIAKI, SAKAMOTO NORIHIRO

  ジェフコーポレーション, Mar. 2018, 栄養, 3(1) (1), 45 - 50, Japanese

  [Refereed]

  Scientific journal


• Casein kinase 2 phosphorylates and stabilizes C/EBPβ in pancreatic β cells

  Tomoko Takai, Tomokazu Matsuda, Yuki Matsuura, Kaho Inoue, Emi Suzuki, Ayumi Kanno, Maki Kimura-Koyanagi, Shun-ichiro Asahara, Naoya Hatano, Wataru Ogawa, Yoshiaki Kido

  Elsevier B.V., Feb. 2018, Biochemical and Biophysical Research Communications, 497(1) (1), 451 - 456, English

  [Refereed]

  Scientific journal


• Casein kinase 2 phosphorylates and stabilizes C/EBPβ in pancreatic β cells

  Tomoko Takai, Tomokazu Matsuda, Yuki Matsuura, Kaho Inoue, Emi Suzuki, Ayumi Kanno, Maki Kimura-Koyanagi, Shun-ichiro Asahara, Naoya Hatano, Wataru Ogawa, Yoshiaki Kido

  Elsevier B.V., Feb. 2018, Biochemical and Biophysical Research Communications, 497(1) (1), 451 - 456, English

  [Refereed]

  Scientific journal


• 金属アレルギー患者に対する管理栄養士による栄養指導の有効性と尿中金属濃度

  三ヶ尻 礼子, 福永 淳, 三好 真琴, 前重 伯壮, 吉岡 愛育, 鷲尾 健, 西山 智司, 正木 太朗, 山本 育子, 高橋 路子, 小川 渉, 木戸 良明, 錦織 千佳子, 宇佐美 眞

  (株)ジェフコーポレーション, Jan. 2018, 日本静脈経腸栄養学会雑誌, 33(Suppl.) (Suppl.), 222 - 222, Japanese

  [Refereed]


• Docosahexaenoic Acid Reduces Palmitic Acid-Induced Endoplasmic Reticulum Stress in Pancreatic .BETA. Cells

  SUZUKI Emi, MATSUDA Tomokazu, KAWAMOTO Takeshi, TAKAHASHI Hiroaki, MIEDA Yusuke, MATSUURA Yuki, TAKAI Tomoko, KANNO Ayumi, KOYANAGI-KIMURA Maki, ASAHARA Shun-Ichiro, INOUE Hiroshi, OGAWA Wataru, KIDO Yoshiaki

  2018, Kobe Journal of Medical Sciences (Web), 64(2) (2), E43‐E55 (WEB ONLY), English

  [Refereed]

  Research institution

  Link to Kobe Univ. Repository (Kernel)


• mTORC1 Signaling: A Double-Edged Sword in Diabetic β c Cells.

  Ardestani A, Lupse B, KIDO YOSHIAKI, Leibowitz G, Maedler K

  2018, Cell Metab, 27, 314 - 331, English

  [Refereed]

  Scientific journal


• 膵β細胞の小胞体ストレス誘導性アポトーシスにおけるCK2βの役割

  井上 佳歩, 高井 智子, 松田 友和, 鈴木 江美, 神野 歩, 木村 真希, 淺原 俊一郎, 木戸 良明

  生命科学系学会合同年次大会運営事務局, Dec. 2017, 生命科学系学会合同年次大会, 2017年度, [1P - 1157], Japanese


• 高脂肪食負荷GCN2欠損マウスの膵島におけるmTORC1シグナル調節機構の解明

  古林 鮎子, 神野 歩, 増田 勝久, 吉冨 理紗, 木村 真希, 松田 友和, 淺原 俊一郎, 木戸 良明

  生命科学系学会合同年次大会運営事務局, Dec. 2017, 生命科学系学会合同年次大会, 2017年度, [2P - 0995], Japanese


• ヒトiPS細胞を用いた膵内分泌細胞への分化誘導法の確立

  山田 瑞姫, 淺原 俊一郎, 下野 名奈子, 田中 孝一, 松田 友和, 木村 真希, 神野 歩, 高井 智子, 鈴木 江美, 青井 貴之, 木戸 良明

  生命科学系学会合同年次大会運営事務局, Dec. 2017, 生命科学系学会合同年次大会, 2017年度, [3P - 0838], Japanese


• MTORC1 Regulates both General Autophagy and Mitophagy Induction after Oxidative Phosphorylation Uncoupling

  Alberto Bartolome, Ana Garcia-Aguilar, Shun-Ichiro Asahara, Yoshiaki Kido, Carlos Guillen, Utpal B. Pajvani, Manuel Benito

  Dec. 2017, MOLECULAR AND CELLULAR BIOLOGY, 37(23) (23), e0044 - 17, English

  [Refereed]

  Scientific journal


• Histone deacetylase regulates insulin signaling via two pathways in pancreatic beta cells

  Yukina Kawada, Shun-ichiro Asahara, Yumiko Sugiura, Ayaka Sato, Ayuko Furubayashi, Mao Kawamura, Alberto Bartolome, Emi Terashi-Suzuki, Tomoko Takai, Ayumi Kanno, Maki Koyanagi-Kimura, Tomokazu Matsuda, Naoko Hashimoto, Yoshiaki Kido

  Sep. 2017, PLOS ONE, 12(9) (9), e0184435, English

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• 2型糖尿病の病態把握におけるMPV(平均血小板容積)の有用性に関する検討

  井上 裕行, 斉藤 真裕美, 胡内 久美子, 吉村 豊, 石田 英和, 中谷 敏也, 淺原 俊一郎, 木戸 良明, 菊池 英亮

  (一社)日本糖尿病学会, Apr. 2017, 糖尿病, 60(Suppl.1) (Suppl.1), S - 141, Japanese


• 膵β細胞の小胞体ストレス誘導性アポトーシスにおけるCK2βの役割

  高井智子, 松田友和, 井上佳歩, 松浦有希, 鈴木江美, 神野歩, 木村真希, 淺原俊一郎, 小川渉, Kido Yoshiaki

  Apr. 2017, 糖尿病, 60(Suppl.1) (Suppl.1), S - 464, Japanese

  Research society


• 脂肪酸が膵β細胞の小胞体に及ぼす影響

  鈴木江美, 松田友和, 川本剛士, 松浦有希, 高井智子, 神野歩, 木村真希, 淺原俊一郎, 小川渉, Kido Yoshiaki

  Apr. 2017, 糖尿病, 60(Suppl.1) (Suppl.1), S - 464, Japanese

  Symposium


• ヒトiPS細胞を用いた2型糖尿病発症機序の解明

  下野名奈子, 淺原俊一郎, 原瑞季, 田中孝一, 松田友和, 木村真希, 神野歩, 高井智子, 鈴木江美, 青井貴之, Kido Yoshiaki

  Apr. 2017, 糖尿病, 60(Suppl.1) (Suppl.1), S - 465, Japanese

  Research society


• 小胞体ストレスと膵β細胞

  高井智子, 松田友和, KIDO YOSHIAKI

  2017, Diabetes Frontier, 28, 193 - 198, Japanese

  [Refereed]

  Scientific journal


• 週１回製剤のアンメットニーズ探索

  松田 友和, 鈴木江美, 高井智子, 野村和弘, 名田高幸, KIDO YOSHIAKI, 横井峰人

  2017, Prog.Med, 37, 1113 - 1122, Japanese

  [Refereed]

  Scientific journal


• Gene-Environment interaction in Type2 Diabetes.

  KIDO YOSHIAKI

  Springer Japan Production Department, 2017, Diabetology International, 8(1) (1), 7 - 13, English

  [Refereed]

  Scientific journal


• Dietary Mung Bean Protein Reduces Hepatic Steatosis, Fibrosis, and Inflammation in Male Mice with Diet-Induced, Nonalcoholic Fatty Liver Disease

  Hitoshi Watanabe, Yuka Inaba, Kumi Kimura, Shun-ichiro Asahara, Yoshiaki Kido, Michihiro Matsumoto, Takayasu Motoyama, Nobuhiko Tachibana, Shuichi Kaneko, Mitsutaka Kohno, Hiroshi Inoue

  Jan. 2017, JOURNAL OF NUTRITION, 147(1) (1), 52 - 60, English

  [Refereed]

  Scientific journal


• Dietary Mung Bean Protein Reduces Hepatic Steatosis, Fibrosis, and Inflammation in Male Mice with Diet-Induced, Nonalcoholic Fatty Liver Disease

  Hitoshi Watanabe, Yuka Inaba, Kumi Kimura, Shun-ichiro Asahara, Yoshiaki Kido, Michihiro Matsumoto, Takayasu Motoyama, Nobuhiko Tachibana, Shuichi Kaneko, Mitsutaka Kohno, Hiroshi Inoue

  Jan. 2017, JOURNAL OF NUTRITION, 147(1) (1), 52 - 60, English

  [Refereed]

  Scientific journal


• The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch

  Mashito Sakai, Tomoko Tujimura-Hayakawa, Takashi Yagi, Hiroyuki Yano, Masaru Mitsushima, Hiroyuki Unoki-Kubota, Yasushi Kaburagi, Hiroshi Inoue, Yoshiaki Kido, Masato Kasuga, Michihiro Matsumoto

  Nov. 2016, NATURE COMMUNICATIONS, 7, English

  [Refereed]

  Scientific journal


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  神野 歩, 増田 勝久, 淺原 俊一郎, 松田 友和, 木村 真希, 廣田 勇士, 横井 伯英, 小川 渉, 清野 進, 春日 雅人, 木戸 良明

  (一社)日本内分泌学会, Apr. 2016, 日本内分泌学会雑誌, 92(1) (1), 242 - 242, Japanese


• 膵β細胞不全関連分子CEBP/βの安定化に対するcasein kinase 2の役割

  高井 智子, 松田 友和, 松浦 有希, 川本 剛士, 淺原 俊一郎, 木村 真希, 神野 歩, 鈴木 江美, 小川 渉, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2016, 糖尿病, 59(Suppl.1) (Suppl.1), S - 158, Japanese


• 生物発光イメージング法による生存細胞内小胞体ストレスの定量化

  鈴木 江美, 松田 友和, 川本 剛士, 松浦 有希, 高井 智子, 神野 歩, 木村 真希, 淺原 俊一郎, 小川 渉, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2016, 糖尿病, 59(Suppl.1) (Suppl.1), S - 353, Japanese


• Central Insulin Action Activates Kupffer Cells by Suppressing Hepatic Vagal Activation via the Nicotinic Alpha 7 Acetylcholine Receptor

  Kumi Kimura, Mamoru Tanida, Naoto Nagata, Yuka Inaba, Hitoshi Watanabe, Mayumi Nagashimada, Tsuguhito Ota, Shun-ichiro Asahara, Yoshiaki Kido, Michihiro Matsumoto, Koji Toshinai, Masamitsu Nakazato, Toshishige Shibamoto, Shuichi Kaneko, Masato Kasuga, Hiroshi Inoue

  Mar. 2016, CELL REPORTS, 14(10) (10), 2362 - 2374, English

  [Refereed]

  Scientific journal


• Central Insulin Action Activates Kupffer Cells by Suppressing Hepatic Vagal Activation via the Nicotinic Alpha 7 Acetylcholine Receptor

  Kumi Kimura, Mamoru Tanida, Naoto Nagata, Yuka Inaba, Hitoshi Watanabe, Mayumi Nagashimada, Tsuguhito Ota, Shun-ichiro Asahara, Yoshiaki Kido, Michihiro Matsumoto, Koji Toshinai, Masamitsu Nakazato, Toshishige Shibamoto, Shuichi Kaneko, Masato Kasuga, Hiroshi Inoue

  Mar. 2016, CELL REPORTS, 14(10) (10), 2362 - 2374, English

  [Refereed]

  Scientific journal


• C/EBPβの蛋白安定化に関与する新規リン酸化部位の同定

  松浦 有希, 松田 友和, 高井 智子, 川本 剛士, 三枝 祐介, 鈴木 江美[寺師], 淺原 俊一郎, 木村 真希[小柳], 神野 歩, 木戸 良明

  (公社)日本生化学会, Dec. 2015, 日本生化学会大会・日本分子生物学会年会合同大会講演要旨集, 88回・38回, [2P1230] - [2P1230], Japanese


• 膵β細胞不全関連分子CEBP/βの安定化に対するcasein kinase βの役割

  高井 智子, 松田 友和, 川本 剛, 松浦 有希, 淺原 俊一郎, 神野 歩, 木村 真希, 鈴木 江美[寺師], 小川 渉, 木戸 良明

  (公社)日本生化学会, Dec. 2015, 日本生化学会大会・日本分子生物学会年会合同大会講演要旨集, 88回・38回, [4T特L - 08(3P1199)], Japanese


• Paternal allelic mutation at the Kcnq1 locus reduces pancreatic beta-cell mass by epigenetic modification of Cdkn1c

  Shun-ichiro Asahara, Hiroaki Etoh, Hiroyuki Inoue, Kyoko Teruyama, Yuki Shibutani, Yuka Ihara, Yukina Kawada, Alberto Bartolome, Naoko Hashimoto, Tomokazu Matsuda, Maki Koyanagi-Kimura, Ayumi Kanno, Yushi Hirota, Tetsuya Hosooka, Kazuaki Nagashima, Wataru Nishimura, Hiroshi Inoue, Michihiro Matsumoto, Michael J. Higgins, Kazuki Yasuda, Nobuya Inagaki, Susumu Seino, Masato Kasuga, Yoshiaki Kido

  Jul. 2015, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 112(27) (27), 8332 - 8337, English

  [Refereed]

  Scientific journal


• Regulation of Pancreatic beta Cell Mass by Cross-Interaction between CCAAT Enhancer Binding Protein beta Induced by Endoplasmic Reticulum Stress and AMP-Activated Protein Kinase Activity

  Tomokazu Matsuda, Hiroaki Takahashi, Yusuke Mieda, Shinobu Shimizu, Takeshi Kawamoto, Yuki Matsuura, Tomoko Takai, Emi Suzuki, Ayumi Kanno, Maki Koyanagi-Kimura, Shun-ichiro Asahara, Alberto Bartolome, Norihide Yokoi, Hiroshi Inoue, Wataru Ogawa, Susumu Seino, Yoshiaki Kido

  Jun. 2015, PLOS ONE, 10(6) (6), e0130757, English

  [Refereed]

  Scientific journal


• Expression of AKR1C3 and CNN3 as markers for detection of lymph node metastasis in colorectal cancer.

  Nakarai C, OSAWA KAYO, Akiyama M, Matsubara N, Ikeuchi H, Yamano T, Hirota S, Tomita N, USAMI MAKOTO, KIDO YOSHIAKI

  Jun. 2015, Clin Exp Med, 15, 333 - 341, English

  [Refereed]

  Scientific journal


• Pathogenesis of Selective Insulin Resistance in Isolated Hepatocytes

  Joshua R. Cook, Fanny Langlet, Yoshiaki Kido, Domenico Accili

  May 2015, JOURNAL OF BIOLOGICAL CHEMISTRY, 290(22) (22), 13972 - 13980, English

  [Refereed]

  Scientific journal


• Pathogenesis of Selective Insulin Resistance in Isolated Hepatocytes

  Joshua R. Cook, Fanny Langlet, Yoshiaki Kido, Domenico Accili

  May 2015, JOURNAL OF BIOLOGICAL CHEMISTRY, 290(22) (22), 13972 - 13980, English

  [Refereed]

  Scientific journal


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  増田 勝久, 神野 歩, 淺原 俊一郎, 吉冨 理紗, 松田 友和, 木村 真希, 渋谷 由紀, 廣田 勇士, 横井 伯英, 春日 雅人, 清野 進, 木戸 良明

  (一社)日本内分泌学会, Apr. 2015, 日本内分泌学会雑誌, 91(1) (1), 274 - 274, Japanese


• 膵β細胞におけるヒストン脱アセチル化酵素HDACの機能解析

  淺原 俊一郎, 杉浦 佑実子, 川田 有希奈, 伊原 佑香, 原 瑞季, 木村 真希, 松田 友和, 清野 進, 小川 渉, 木戸 良明

  (一社)日本内分泌学会, Apr. 2015, 日本内分泌学会雑誌, 91(1) (1), 318 - 318, Japanese


• C/EBPβの蛋白安定化に関与する新規リン酸化部位の同定

  川本 剛士, 松田 友和, 三枝 祐介, 高井 智子, 松浦 有希, 淺原 俊一郎, 木村 真希, 神野 歩, 木戸 良明

  (一社)日本内分泌学会, Apr. 2015, 日本内分泌学会雑誌, 91(1) (1), 319 - 319, Japanese


• DPP-4阻害薬MK-626が膵β細胞特異的mTORC1活性亢進モデルマウスに及ぼす影響

  木村 真希, 森田 愛梨, 三上 智子, 神野 歩, 松田 友和, 淺原 俊一郎, 清野 進, 小川 渉, 木戸 良明

  (一社)日本内分泌学会, Apr. 2015, 日本内分泌学会雑誌, 91(1) (1), 352 - 352, Japanese


• 膵β細胞不全関連因子C/EBPβの発現制御機構の解明

  高井 智子, 松田 友和, 川本 剛士, 松浦 有希, 三枝 祐介, 鈴木 江美, 淺原 俊一郎, 木村 真希, 神野 歩, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2015, 糖尿病, 58(Suppl.1) (Suppl.1), S - 149, Japanese


• 膵β細胞におけるp38経路の活性化は膵島の慢性炎症を惹起することにより膵β細胞不全の病態形成に関与する

  森田 愛梨, 細岡 哲也, 竹村 侑己, 木村 真希, 鈴木 夏実, 淺原 俊一郎, 神野 歩, 松田 友和, 清野 進, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2015, 糖尿病, 58(Suppl.1) (Suppl.1), S - 262, Japanese


• ヒストン脱アセチル化酵素(HDACs)による膵β細胞量調節機構の解析

  杉浦 佑実子, 淺原 俊一郎, 川田 有希奈, 佐藤 綾香, 木村 真希, 松田 友和, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2015, 糖尿病, 58(Suppl.1) (Suppl.1), S - 443, Japanese


• 膵β細胞における細胞周期調節因子p57の機能解析

  原 瑞季, 淺原 俊一郎, 伊原 佑香, 井上 裕行, 照山 杏子, 松田 友和, 木村 真希, 中山 敬一, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2015, 糖尿病, 58(Suppl.1) (Suppl.1), S - 263, Japanese


• Growth Arrest and DNA Damage-Inducible 34 Regulates Liver Regeneration in Hepatic Steatosis in Mice

  Yuka Inaba, Tomoko Furutani, Kumi Kimura, Hitoshi Watanabe, Sanae Haga, Yoshiaki Kido, Michihiro Matsumoto, Yasuhiko Yamamoto, Kenichi Harada, Shuichi Kaneko, Seiichi Oyadomari, Michitaka Ozaki, Masato Kasuga, Hiroshi Inoue

  Apr. 2015, HEPATOLOGY, 61(4) (4), 1343 - 1356, English

  [Refereed]

  Scientific journal


• Compensatory hyperinsulinemia in high-fat diet-induced obese mice is associated with enhanced insulin translation in islets

  Ayumi Kanno, Shun-ichiro Asahara, Katsuhisa Masuda, Tomokazu Matsuda, Maki Kimura-Koyanagi, Susumu Seino, Wataru Ogawa, Yoshiaki Kido

  Mar. 2015, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 458(3) (3), 681 - 686, English

  [Refereed]

  Scientific journal


• 【糖尿病治療の経口薬up to date】これらの薬剤のみで不十分な際に、相乗効果を期待して加える薬剤は、その理由は? SU薬

  木村 真希, 松田 友和, 木戸 良明

  (株)医学出版, Feb. 2015, 月刊糖尿病, 7(2) (2), 88 - 94, Japanese


• A case of hemiplegia with hypoglycemia possibly associated with hemodynamic change.

  Matsuda T, Iwasaki M, Yoshioka N, Hirota Y, Hamaguchi H, KIDO YOSHIAKI, Sakaguchi K, Ogawa W

  Springer Japan, 2015, Diabetol Int, 6(4) (4), 336 - 340, English

  [Refereed]

  Scientific journal


• Pancreatic beta-Cell Failure Mediated by mTORC1 Hyperactivity and Autophagic Impairment

  Alberto Bartolome, Maki Kimura-Koyanagi, Shun-Ichiro Asahara, Carlos Guillen, Hiroyuki Inoue, Kyoko Teruyama, Shinobu Shimizu, Ayumi Kanno, Ana Garcia-Aguilar, Masato Koike, Yasuo Uchiyama, Manuel Benito, Tetsuo Noda, Yoshiaki Kido

  Sep. 2014, DIABETES, 63(9) (9), 2996 - 3008, English

  [Refereed][Invited]

  Scientific journal


• Pancreatic beta-Cell Failure Mediated by mTORC1 Hyperactivity and Autophagic Impairment

  Alberto Bartolome, Maki Kimura-Koyanagi, Shun-Ichiro Asahara, Carlos Guillen, Hiroyuki Inoue, Kyoko Teruyama, Shinobu Shimizu, Ayumi Kanno, Ana Garcia-Aguilar, Masato Koike, Yasuo Uchiyama, Manuel Benito, Tetsuo Noda, Yoshiaki Kido

  Sep. 2014, DIABETES, 63(9) (9), 2996 - 3008, English

  [Refereed]

  Scientific journal


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  神野 歩, 吉冨 理紗, 増田 勝久, 淺原 俊一郎, 松田 友和, 木村 真希, 澁谷 由紀, 廣田 勇士, 横井 伯英, 春日 雅人, 清野 進, 木戸 良明

  (一社)日本内分泌学会, Apr. 2014, 日本内分泌学会雑誌, 90(1) (1), 252 - 252, Japanese


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  増田 勝久, 神野 歩, 吉冨 理紗, 淺原 俊一郎, 松田 友和, 木村 真希, 渋谷 由紀, 廣田 勇士, 横井 伯英, 春日 雅人, 清野 進, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2014, 糖尿病, 57(Suppl.1) (Suppl.1), S - 141, Japanese


• AMPK活性依存的なC/EBPβの発現調節による膵β細胞量制御機構

  三枝 祐介, 松田 友和, 高橋 宏昌, 鈴木 江美, 川本 剛士, 淺原 俊一郎, 木村 真希, 神野 歩, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2014, 糖尿病, 57(Suppl.1) (Suppl.1), S - 263, Japanese


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  神野 歩, 吉冨 理紗, 増田 勝久, 淺原 俊一郎, 松田 友和, 木村 真希, 渋谷 由紀, 廣田 勇士, 横井 伯英, 春日 雅人, 清野 進, 木戸 良明

  日本臨床分子医学会, Apr. 2014, 日本臨床分子医学会学術総会プログラム・抄録集, 51回, 78 - 78, Japanese


• 膵β細胞のKcnq1遺伝子領域におけるエピジェネティクス制御機構の解析

  淺原 俊一郎, 照山 杏子, 井上 裕行, 伊原 佑香, 江藤 博昭, 川田 有希奈, 松田 友和, 春日 雅人, 清野 進, 木戸 良明

  (一社)日本内分泌学会, Apr. 2014, 日本内分泌学会雑誌, 90(1) (1), 267 - 267, Japanese


• 膵β細胞のKcnq1遺伝子領域におけるエピジェネティクス制御機構の解析

  伊原 佑香, 淺原 俊一郎, 照山 杏子, 井上 裕行, 江藤 博昭, 木村 真希, 松田 友和, 春日 雅人, 清野 進, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2014, 糖尿病, 57(Suppl.1) (Suppl.1), S - 142, Japanese


• Atomistic structure of a spinel Li4Ti5O 12(111) surface elucidated by scanning tunneling microscopy and medium energy ion scattering spectrometry

  Mitsunori Kitta, Taishi Matsuda, Yasushi Maeda, Tomoki Akita, Shingo Tanaka, Yoshiaki Kido, Masanori Kohyama

  Jan. 2014, Surface Science, 619, 5 - 9, English

  [Refereed]

  Scientific journal


• Contribution of insulin signaling to the regulation of pancreatic beta-cell mass during the catch-up growth period in a low birth weight mouse model

  Yuri Yoshida, Megumi Fuchita, Maki Kimura-Koyanagi, Ayumi Kanno, Tomokazu Matsuda, Shun-ichiro Asahara, Naoko Hashimoto, Takayuki Isagawa, Wataru Ogawa, Hiroyuki Aburatani, Tetsuo Noda, Susumu Seino, Masato Kasuga, Yoshiaki Kido

  Springer-Verlag Tokyo, 2014, Diabetology International, 5(1) (1), 43 - 52, English

  [Refereed]

  Scientific journal


• 卵巣奇形腫に対して発症早期に腹腔鏡手術を施行し経過良好であった抗NMDAR抗体関連脳炎の１症例

  Kumano Masafumi, 蝦名 康彦, Kumano Masafumi, Yamaguchi Kohei, Chiba Koji, Tamiya Hiroko, Kido Yoshiaki, Junya Furukawa, 宮崎 彰, 山崎 友維, 藤澤正人, Kenichi Harada, 鄭 裕元, 白川 得朗, Mototsugu Muramaki, 西川昌友, 牧原 夏子, Hideaki Miyake, 宮原 義也, 古川順也, Masato Fujisawa, 原田健一, 新谷 潔, 中林 幸士, 日向信之, 松岡 正造, 村蒔基次, 三宅秀明, 上中建, 横田 一郎, 藤澤正人, 苅田 典生, 田中 惠, Yamada Hideto

  2014, 日本産科婦人科内視鏡学会雑誌, 40, Japanese

  [Refereed]

  Scientific journal


• Role of gold nanoclusters supported on TiO2(110) model catalyst in CO oxidation reaction

  Anton Visikovskiy, Kei Mitsuhara, Yoshiaki Kido

  Nov. 2013, Journal of Vacuum Science and Technology A: Vacuum, Surfaces and Films, 31(6) (6), English

  [Refereed]

  Scientific journal


• 膵β細胞増殖機構におけるエピジェネティクス修飾の解析

  川田 有希奈, 井上 裕行, 小柳 真希, 松田 友和, 淺原 俊一郎, 木戸 良明

  (一社)日本臨床検査医学会, Sep. 2013, 臨床病理, 61(補冊) (補冊), 280 - 280, Japanese


• Histidine Augments the Suppression of Hepatic Glucose Production by Central Insulin Action

  Kumi Kimura, Yusuke Nakamura, Yuka Inaba, Michihiro Matsumoto, Yoshiaki Kido, Shun-ichiro Asahara, Tomokazu Matsuda, Hiroshi Watanabe, Akifumi Maeda, Fuyuhiko Inagaki, Chisato Mukai, Kiyoshi Takeda, Shizuo Akira, Tsuguhito Ota, Hajime Nakabayashi, Shuichi Kaneko, Masato Kasuga, Hiroshi Inoue

  Jul. 2013, DIABETES, 62(7) (7), 2266 - 2277, English

  [Refereed]

  Scientific journal


• The structure of SrTiO3(001)-2 × 1 surface analyzed by high-resolution medium energy ion scattering coupled with ab initio calculations

  Taishi Matsuda, Yuki Yoshida, Kei Mitsuhara, Yoshiaki Kido

  Jun. 2013, Journal of Chemical Physics, 138(24) (24), English

  [Refereed]

  Scientific journal


• Constitutive activation of Rac1 in pancreatic β cells facilitates F-actin depolymerization but exerts no influence on the increase of pancreatic β cell mass and facilitation of insulin secretion.

  Yuki Shibutani, Shun-Ichiro Asahara, Kyoko Teruyama, Hiroyuki Inoue, Tomokazu Matsuda, Susumu Seino, Yoshiaki Kido

  Insulin secretion from pancreatic β cells has an important role in the onset of type 2 diabetes. Insulin secretion from pancreatic β cells is regulated by pancreatic β cell mass and their insulin secretory function. By using pancreatic β cell-specific Rac1-knockout mice, we recently showed that Rac1 deletion, even with no reduction in pancreatic β cell mass, inhibits F-actin depolymerization, which causes insulin secretion to decline. However, the effect of Rac1 deficiency on the growth and apoptosis of pancreatic β cells was not clarified. Further, the effect of constitutive Rac1 activation on the secretion of insulin from pancreatic β cells has not been studied. Here, we used pancreatic islets isolated from pancreatic β cell-specific Rac1-knockout mice to evaluate the growth and apoptosis of pancreatic β cells. We found that Rac1 deficiency does not influence the growth or apoptosis of pancreatic β cells. Further, when a constitutively activated form of Rac1 (G12V) is expressed, F-actin depolymerization was increased in the pancreatic β cell lines, which had no effect on pancreatic β cell growth or glucose-stimulated insulin secretion. These findings indicate that excessive Rac1 expression or activation in pancreatic β cells facilitates F-actin depolymerization, but has no effect on insulin secretion.

  May 2013, The Kobe journal of medical sciences, 59(3) (3), E72-80 - 80, English, Domestic magazine

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Ras-related C3 botulinum toxin substrate 1 (RAC1) regulates glucose-stimulated insulin secretion via modulation of F-actin

  S. Asahara, Y. Shibutani, K. Teruyama, H. Y. Inoue, Y. Kawada, H. Etoh, T. Matsuda, M. Kimura-Koyanagi, N. Hashimoto, M. Sakahara, W. Fujimoto, H. Takahashi, S. Ueda, T. Hosooka, T. Satoh, H. Inoue, M. Matsumoto, A. Aiba, M. Kasuga, Y. Kido

  May 2013, DIABETOLOGIA, 56(5) (5), 1088 - 1097, English

  [Refereed]

  Scientific journal


• Catalytic activity of Pt/TaB2(0001) for the oxygen reduction reaction

  Eishiro Toyoda, Ryosuke Jinnouchi, Tetsu Ohsuna, Tatsuya Hatanaka, Takashi Aizawa, Shigeki Otani, Yoshiaki Kido, Yu Morimoto

  Apr. 2013, Angewandte Chemie - International Edition, 52(15) (15), 4137 - 4140, English

  [Refereed]

  Scientific journal


• DPP4阻害薬MK-626が膵β細胞特異mTORC1活性亢進モデルマウスに及ぼす影響

  三上 智子, 小柳 真希, 松田 友和, 神野 歩, 淺原 俊一郎, 春日 雅人, 清野 進, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2013, 糖尿病, 56(Suppl.1) (Suppl.1), S - 188, Japanese


• インスリノーマにおけるインスリン分泌特性と遺伝子発現の解析

  小柳 真希, 松田 友和, 廣田 勇士, 橋本 尚子, 淺原 俊一郎, 中村 友昭, 木戸 良明, 坂口 一彦, 小川 渉, 清野 進

  (一社)日本内科学会, Feb. 2013, 日本内科学会雑誌, 102(Suppl.) (Suppl.), 214 - 214, Japanese


• Enhanced and correlated lattice vibrations of relaxed Cu(001) surface studied by high-resolution medium energy ion scattering

  Taishi Matsuda, Yuta Aiba, Jyunki Morimoto, Kei Mitsuhara, Yoshiaki Kido

  Elsevier B.V., 2013, Nuclear Instruments and Methods in Physics Research, Section B: Beam Interactions with Materials and Atoms, 308, 100 - 108, English

  [Refereed]

  Scientific journal


• 短時間および長時間作用型GLP-1受容体作動薬が食行動に及ぼす影響

  Yoshiaki Kido, 城内繭子, 別當憲子, 穴倉弘枝, 南美樹, 松田友和, 宇佐美勝, 池田弘毅, 池田正毅

  2013, 日本病態栄養学会誌, 16巻, 407 - 414, English

  [Refereed]

  Scientific journal


• XRCC3 Gene Polymorphism Is Associated with Survival in Japanese Lung Cancer Patients

  Kayo Osawa, Chiaki Nakarai, Kazuya Uchino, Masahiro Yoshimura, Noriaki Tsubota, Juro Takahashi, Yoshiaki Kido

  Dec. 2012, INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 13(12) (12), 16658 - 16667, English

  [Refereed]

  Scientific journal


• DPP4 inhibitor vildagliptin preserves β-cell mass through amelioration of endoplasmic reticulum stress in C/EBPB transgenic mice.

  Shinobu Shimizu, Tetsuya Hosooka, Tomokazu Matsuda, Shun-ichiro Asahara, Maki Koyanagi-Kimura, Ayumi Kanno, Alberto Bartolome, Hiroaki Etoh, Megumi Fuchita, Kyoko Teruyama, Hiroaki Takahashi, Hiroyuki Inoue, Yusuke Mieda, Naoko Hashimoto, Susumu Seino, Yoshiaki Kido

  The development of type 2 diabetes is accompanied by a progressive decline in β-cell mass and function. Vildagliptin, a dipeptidyl peptidase 4 inhibitor, is representative of a new class of antidiabetic agents that act through increasing the expression of glucagon-like peptide-1. The protective effect of this agent on β cells was studied in diabetic mice. Diabetic pancreatic β cell-specific C/EBPB transgenic (TG) mice exhibit decreased β-cell mass associated with increased apoptosis, decreased proliferation, and aggravated endoplasmic reticulum (ER) stress. Vildagliptin was orally administered to the TG mice for a period of 24 weeks, and the protective effects of this agent on β cells were examined, along with the potential molecular mechanism of protection. Vildagliptin ameliorated hyperglycemia in TG mice by increasing the serum concentration of insulin and decreasing the serum concentration of glucagon. This agent also markedly increased β-cell mass, improved aggravated ER stress, and restored attenuated insulin/IGF1 signaling. A decrease in pancreatic and duodenal homeobox 1 expression was also observed in β cells isolated from our mouse model, but this was also restored by vildagliptin treatment. The expression of C/EBPB protein, but not mRNA, was unexpectedly downregulated in vildagliptin-treated TG mice and in exenatide-treated MIN6 cells. Activation of the GLP1 pathway induced proteasome-dependent C/EBPB degradation in β cells as the proteasome inhibitor MG132 restored the downregulation of C/EBPB protein by exenatide. Vildagliptin elicits protective effects on pancreatic β cells, possibly through C/EBPB degradation, and has potential for preventing the progression of type 2 diabetes.

  Oct. 2012, Journal of molecular endocrinology, 49(2) (2), 125 - 35, English, International magazine

  [Refereed]

  Scientific journal


• Significance of ELF3 mRNA Expression for Detection of Lymph Node Metastases of Colorectal Cancer

  Chiaki Nakarai, Kayo Osawa, Nagahide Matsubara, Hiroki Ikeuchi, Tomoki Yamano, Shu Okamura, Shingo Kamoshida, Akimitsu Tsutou, Juro Takahashi, Kazushige Ejiri, Seiichi Hirota, Naohiro Tomita, Yoshiaki Kido

  Sep. 2012, ANTICANCER RESEARCH, 32(9) (9), 3753 - 3758, English

  [Refereed]

  Scientific journal


• Cross sections for medium energy He ions scattered from Hf and Au atoms

  Tomoaki Nishimura, Kei Mitsuhara, Anton Visikovskiy, Yoshiaki Kido

  Jun. 2012, Nuclear Instruments and Methods in Physics Research, Section B: Beam Interactions with Materials and Atoms, 280, 5 - 9, English

  [Refereed]

  Scientific journal


• 膵β細胞特異的C/EBPβトランスジェニックマウスに対するビルダグリプチンの膵β細胞保護効果に関する検討

  松田 友和, 清水 忍, 細岡 哲也, 浅原 俊一郎, 高橋 宏昌, 木村 真希, 清野 進, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2012, 糖尿病, 55(Suppl.1) (Suppl.1), S - 298, Japanese


• 2型糖尿病発症におけるeIF2αキナーゼGCN2の機能解析

  神野 歩, 吉冨 理紗, 淺原 俊一郎, 松田 友和, 木村 真希, 渋谷 由紀, 春日 雅人, 清野 進, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2012, 糖尿病, 55(Suppl.1) (Suppl.1), S - 298, Japanese


• Kcnq1遺伝子領域におけるエピジェネティクス制御が膵β細胞量に及ぼす影響の解析

  照山 杏子, 淺原 俊一郎, 江藤 博昭, 井上 裕行, 松田 友和, 春日 雅人, 清野 進, 木戸 良明

  (一社)日本糖尿病学会, Apr. 2012, 糖尿病, 55(Suppl.1) (Suppl.1), S - 297, Japanese


• Kcnq1遺伝子領域におけるエピジェネティクス制御が膵β細胞量に及ぼす影響の解析

  照山 杏子, 淺原 俊一郎, 江藤 博昭, 井上 裕行, 松田 友和, 清野 進, 春日 雅人, 木戸 良明

  日本臨床分子医学会, Apr. 2012, 日本臨床分子医学会学術総会プログラム・抄録集, 49回, 76 - 76, Japanese


• CITED2 links hormonal signaling to PGC-1 alpha acetylation in the regulation of gluconeogenesis

  Mashito Sakai, Michihiro Matsumoto, Tomoko Tujimura, Cao Yongheng, Tetsuya Noguchi, Kenjiro Inagaki, Hiroshi Inoue, Tetsuya Hosooka, Kazuo Takazawa, Yoshiaki Kido, Kazuki Yasuda, Ryuji Hiramatsu, Yasushi Matsuki, Masato Kasuga

  Apr. 2012, NATURE MEDICINE, 18(4) (4), 612 - 617, English

  [Refereed]

  Scientific journal


• Association between Polymorphisms in UDP-glucuronosyltransferase 1A6 and 1A7 and Colorectal Cancer Risk

  Kayo Osawa, Chiaki Nakarai, Minami Akiyama, Ryuta Hashimoto, Akimitsu Tsutou, Juro Takahashi, Yuko Takaoka, Shiro Kawamura, Etsuji Shimada, Kenichi Tanaka, Masaya Kozuka, MasahiroYamamoto, Yoshiaki Kido

  2012, ASIAN PACIFIC JOURNAL OF CANCER PREVENTION, 13(5) (5), 2311 - 2314, English

  [Refereed]

  Scientific journal


• A calculation model for serum ionized calcium based on an equilibrium equation for complexation.

  Susumu Takano, Hiroshi Kaji, Fujio Hayashi, Kanae Higashiguchi, Sachie Joukei, Yoshiaki Kido, Juro Takahashi, Kayo Osawa

  Measurement of ionized calcium is more important than measurement of total calcium in serum samples. In the present study, equations were derived from complexation and acid dissociation equilibrium equations, and were used to determine the concentration of ionized calcium from the observed serum concentrations of total calcium, albumin, total protein, and inorganic phosphate. The ionized calcium concentration was calculated in 67 serum samples from healthy subjects and 34 outpatients previously identified as having abnormal serum calcium levels. The correlation coefficient between our method (y) and the calcium-ion-selective electrode method (x) was 0.953 and the linear regression equation was y = 0.97x at pH 7.4 with a factor of α = 0.21, which was based on the differences between the concentrations of calcium phosphorus compounds obtained by the electrode method and by calculation. The developed calculation is as useful and accurate as the electrode method, and therefore extremely useful for clinical diagnoses.

  2012, Analytical chemistry insights, 7, 23 - 30, English, International magazine

  [Refereed]

  Scientific journal


• Endoplasmic Reticulum Stress Inhibits STAT3-Dependent Suppression of Hepatic Gluconeogenesis via Dephosphorylation and Deacetylation

  Kumi Kimura, Tomoko Yamada, Michihiro Matsumoto, Yoshiaki Kido, Tetsuya Hosooka, Shun-ichiro Asahara, Tomokazu Matsuda, Tsuguhito Ota, Hiroshi Watanabe, Yoshimichi Sai, Kenichi Miyamoto, Shuichi Kaneko, Masato Kasuga, Hiroshi Inoue

  Jan. 2012, DIABETES, 61(1) (1), 61 - 73, English

  Scientific journal


• A Case of an Elderly Patient with Slowly Progressive Type 1 Diabetes Who Developed Severe Nonocclusive Mesenteric Ischemia without Predisposing Events

  Kenta Hara, Hisafumi Yasuda, Takashi Arai, Sonoko Miyoshi, Osamu Kubokawa, Hiroyuki Mori, Taichi Akisaki, Yoshiaki Kido, Koichi Yokono, Hozuka Akita

  2012, INTERNAL MEDICINE, 51(9) (9), 1065 - 1068, English

  [Refereed]

  Scientific journal


• The d-band structure of Pt nanoclusters correlated with the catalytic activity for an oxygen reduction reaction

  Eishiro Toyoda, Ryosuke Jinnouchi, Tatsuya Hatanaka, Yu Morimoto, Kei Mitsuhara, Anton Visikovskiy, Yoshiaki Kido

  Nov. 2011, Journal of Physical Chemistry C, 115(43) (43), 21236 - 21240, English

  [Refereed]

  Scientific journal


• 2型糖尿病関連遺伝子Kcnq1領域の膵β細胞に及ぼす影響の検討

  江藤 博昭, 淺原 俊一郎, 照山 杏子, 井上 裕行, 小柳 真希, 渋谷 由紀, 松田 友和, 長嶋 一昭, 西村 渉, 安田 和基, 稲垣 暢也, 清野 進, 春日 雅人, 木戸 良明

  (一社)日本肥満学会, Sep. 2011, 肥満研究, 17(Suppl.) (Suppl.), 160 - 160, Japanese


• Oxygen deficiency and excess of rutile titania (1 1 0) surfaces analyzed by ion scattering coupled with elastic recoil detection

  Kei Mitsuhara, Taishi Matsuda, Hideki Okumura, Anton Visikovskiy, Yoshiaki Kido

  Aug. 2011, Nuclear Instruments and Methods in Physics Research, Section B: Beam Interactions with Materials and Atoms, 269(16) (16), 1859 - 1864, English

  [Refereed]

  Scientific journal


• Ablation of TSC2 Enhances Insulin Secretion by Increasing the Number of Mitochondria through Activation of mTORC1

  Maki Koyanagi, Shun-ichiro Asahara, Tomokazu Matsuda, Naoko Hashimoto, Yutaka Shigeyama, Yuki Shibutani, Ayumi Kanno, Megumi Fuchita, Tomoko Mikami, Tetsutya Hosooka, Hiroshi Inoue, Michihiro Matsumoto, Masato Koike, Yasuo Uchiyama, Tetsuo Noda, Susumu Seino, Masato Kasuga, Yoshiaki Kido

  Aug. 2011, PLOS ONE, 6(8) (8), English

  [Refereed]

  Scientific journal


• Electronic d-band properties of gold nanoclusters grown on amorphous carbon

  Anton Visikovskiy, Hisashi Matsumoto, Kei Mitsuhara, Toshitaka Nakada, Tomoki Akita, Yoshiaki Kido

  Apr. 2011, Physical Review B - Condensed Matter and Materials Physics, 83(16) (16), English

  [Refereed]

  Scientific journal


• CITED2 links hormonal signaling to PGC-1α acetylation in regulation of gluconeogenesis

  Koyanagi M, Asahara S, Matsuda T, Hashimoto N, Shigeyama Y, Shibutani Y, Kanno A, Fuchita M, Mikami T, Hosooka T, Inoue H, Matsumoto M, Koike M, Uchiyama Y, Noda T, Seino S, Kasuga M, Kido Yoshiaki

  2011, PLoS ONE, Vol. 6, pp. e23238, English

  [Refereed]

  Scientific journal


• Elastic Recoil Detection Analysis (ERDA) of hydrogen near solid surfaces

  Yoshiaki Kido

  2010, Journal of the Vacuum Society of Japan, 53(10) (10), 608 - 613, Japanese

  [Refereed]

  Scientific journal


• ERストレスと膵β細胞

  松田友和, Kido Yoshiaki

  2010, Diabetes Frontier, 21, 437 - 441, Japanese

  [Refereed]

  Scientific journal


• APEX1 Asp148Glu Gene Polymorphism is a Risk Factor for Lung Cancer in Relation to Smoking in Japanese

  Kayo Osawa, Aiko Miyaishi, Kazuya Uchino, Yasunori Osawa, Natsuko Inoue, Chiaki Nakarai, Akimitsu Tsutou, Yoshiaki Kido, Masahiro Yoshimura, Noriaki Tsubota, Juro Takahashi

  2010, ASIAN PACIFIC JOURNAL OF CANCER PREVENTION, 11(5) (5), 1181 - 1186, English

  [Refereed]

  Scientific journal


• Ablation of C/EBP beta alleviates ER stress and pancreatic beta cell failure through the GRP78 chaperone in mice

  Tomokazu Matsuda, Yoshiaki Kido, Shun-ichiro Asahara, Tsuneyasu Kaisho, Takashi Tanaka, Naoko Hashimoto, Yutaka Shigeyama, Akihiko Takeda, Tae Inoue, Yuki Shibutani, Maki Koyanagi, Tetsuya Hosooka, Michihiro Matsumoto, Hiroshi Inoue, Tohru Uchida, Masato Koike, Yasuo Uchiyama, Shizuo Akira, Masato Kasuga

  Jan. 2010, JOURNAL OF CLINICAL INVESTIGATION, 120(1) (1), 115 - 126, English

  [Refereed]

  Scientific journal


• Effect of intrauterine undernutrition during late gestation on pancreatic beta cell mass

  Tae Inoue, Yoshiaki Kido, Shun-ichiro Asahara, Tomokazu Matsuda, Yuki Shibutani, Maki Koyanagi, Masato Kasuga

  Dec. 2009, BIOMEDICAL RESEARCH-TOKYO, 30(6) (6), 325 - 330, English

  [Refereed]

  Scientific journal


• 膵β細胞におけるmTORシグナルとミトコンドリア機能の検討

  小柳 真希, 木戸 良明, 浅原 俊一郎, 茂山 豊, 松田 友和, 竹田 章彦, 井上 妙, 渋谷 由紀, 清野 進, 春日 雅人

  日本臨床分子医学会, Apr. 2009, 日本臨床分子医学会学術総会プログラム・抄録集, 46回, 73 - 73, Japanese


• 膵β細胞におけるmTORシグナルとミトコンドリア機能の検討

  小柳 真希, 木戸 良明, 浅原 俊一郎, 茂山 豊, 松田 友和, 竹田 章彦, 井上 妙, 渋谷 由紀, 清野 進, 春日 雅人

  (一社)日本糖尿病学会, Apr. 2009, 糖尿病, 52(Suppl.1) (Suppl.1), S - 217, Japanese


• Increased ribosomal biogenesis induces pancreatic beta cell failure in mice model of type 2 diabetes

  Shun-ichiro Asahara, Tomokazu Matsuda, Yoshiaki Kido, Masato Kasuga

  Apr. 2009, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 381(3) (3), 367 - 371, English

  [Refereed]

  Scientific journal


• Pancreatic beta cell mass preserved in heterozygous PDK1 knockout mice

  Takeda A, Kido Yoshiaki, Hashimoto N, Noda T, Kasuga M

  Sep. 2008, Kobe J Med Sci, 54(3) (3), E183 - 90, English

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Biphasic response of pancreatic beta-cell mass to ablation of tuberous sclerosis complex 2 in mice

  Yutaka Shigeyama, Toshiyuki Kobayashi, Yoshiaki Kido, Naoko Hashimoto, Shun-ichiro Asahara, Tomokazu Matsuda, Akihiko Takeda, Tae Inoue, Yuki Shibutani, Maki Koyanagi, Tohru Uchida, Maki Inoue, Okio Hino, Masato Kasuga, Tetsuo Noda

  May 2008, MOLECULAR AND CELLULAR BIOLOGY, 28(9) (9), 2971 - 2979, English

  [Refereed]

  Scientific journal


• Surface cesium concentration and secondary ion emission from Si 1-xGex bombarded by Cs+

  Akira Mikami, Tetsuaki Okazawa, Yoshiaki Kido

  Apr. 2008, Japanese Journal of Applied Physics, 47(4) (4), 2234 - 2237, English

  [Refereed]

  Scientific journal


• Dietary Self-management Behavior and Actual Energy Intake Analyzed from Individual Type 2 Diabetic Patient Clinical Indices

  TARU Chiemi, NAKAWATASE Yuri, TSUTOU Akimitsu, TAMORI Yoshikazu, NOGUCHI Tetsuya, KIDO Yoshiaki, OHARA Tsuyoshi, OGAWA Wataru, MIYAWAKI Ikuko

  We studied the relationship between dietary self-management behavior and actual energy intake by Type 2 diabetic individuals based on clinical backgrounds and profiles of gender, age, HbA₁c, body mass index (BMI), and waist size. Subjects were 99 men and 77 women. Using data from the dietary self-management behavior questionnaire (DSBQ) and semiquantitative food frequency questionnaire, which lists 122 dishes, we initially divided clinical profiles into two groups. We then assessed the rank correlation coefficient between DSBQ factors and dietary intake using Student's t-test and Spearman's technique. We noted three trends: (1) Men aged <60 showed a noticeably low frequency of behavior such as “Device to enhance satisfaction during meals,” “Device to reduce the use of high-calorie seasoning,” and “Device to eat tasty food while maintaining nutritional balance,” Similarly, those with a BMI of >25 and a waist of >85 cm demonstrated a noticeably low frequency of behavior such as “Device to avoid excessive food intake,” “Device to enhance satisfaction during meals,” and “Device to eat tasty food while maintaining nutritional balance,” consequently reflected in increased dietary intake. (2) Women with HbA₁c <7.0% showed a noticeably high frequency of behavior such as “Device to reduce the amount of cooking salt,” consequently reflected in decreased dietary intake. Women with a BMI of >25 and a waist of >90 cm showed a high frequency of “Behavior that each allows one's own value system to take priority even if it means eating inappropriate food” in behavior to cope with factors interfering with dietary regimens, consequently reflected in increased dietary intake. Results suggest that it is important for the sake of good care to point out each own characteristics of self-management behavior using the DSBQ.

  THE JAPAN DIABETES SOCIETY, 2008, Journal of the Japan Diabetes Society, 51(2) (2), 125 - 138, Japanese

  [Refereed]


• Reduced insulin signaling and endoplasmic reticulum stress act synergistically to deteriorate pancreatic beta cell function.

  Matsuda T, Kido Yoshiaki, Uchida T, Kasuga M

  2008, Kobe J Med Sci, Vol. 54, pp. E114-121, English

  [Refereed]

  Scientific journal


• 膵β細胞の数・大きさの制御とインスリン分泌－mTORを中心に－

  Kido Yoshiaki

  Dec. 2007, 第30回日本分子生物学会年会 第80回日本生化学会大会 合同大会, 巻, , pp. 73-73, Japanese

  International conference proceedings


• Development of an evaluation scale for self-management behavior related to physical activity of type 2 diabetic patients

  Yuri Nakawatase, Chiemi Taru, Akimitsu Tsutou, Hideyuki Shiotani, Yoshiaki Kido, Takeshi Ohara, Wataru Ogawa, Ikuko Miyawaki

  Nov. 2007, DIABETES CARE, 30(11) (11), 2843 - 2848, English

  [Refereed]

  Scientific journal


• Unique mechanisms of growth regulation and tumor suppression upon Apc inactivation in the pancreas

  Alessandra Strom, Claire Bonal, Ruth Ashery-Padan, Naoko Hashimoto, M. Luisa Campos, Andreas Trumpp, Tetsuo Noda, Yoshiaki Kido, Francisco X. Real, Fabrizio Thorel, Pedro L. Herrera

  Aug. 2007, DEVELOPMENT, 134(15) (15), 2719 - 2725, English

  [Refereed]

  Scientific journal


• Analysis of compensatory beta-cell response in mice with combined mutations of Insr and Irs2

  Jane J. Kim, Yoshiaki Kido, Philipp E. Scherer, Morris F. White, Domenico Accili

  Jun. 2007, AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 292(6) (6), E1694 - E1701, English

  [Refereed]

  Scientific journal


• PI3Kおよび関連シグナル伝達分子の機能 グルコース代謝におけるPDK1の役割(Role of PDK1 in Glucose Metabolism)(英語)

  Kido Yoshiaki

  May 2007, 日本発生生物学会・日本細胞生物学会合同大会要旨集40回・59回, 巻, , pp. 15-15, Japanese

  International conference proceedings


• 膵β細胞量調節因子としてのTSC2の役割 遺伝子改変マウスを用いた検討

  Kido Yoshiaki

  Apr. 2007, 糖尿病, 50巻, Suppl.1, pp. S-212, Japanese

  International conference proceedings


• 妊娠後期の子宮内低栄養が膵β細胞に及ぼす影響

  Kido Yoshiaki

  Apr. 2007, 糖尿病, 50巻, Suppl.1, pp. S-214, Japanese

  International conference proceedings


• 小胞体ストレスにより惹起される膵β細胞不全におけるC/EBPβの役割

  Kido Yoshiaki

  Apr. 2007, 日本内分泌学会雑誌, 83巻, 1号, pp. 89-89, Japanese

  International conference proceedings


• 2型糖尿病の膵β細胞異常(機能・量) 糖尿病発症における膵β細胞量の異常

  Kido Yoshiaki

  Apr. 2007, 糖尿病, 50巻, Suppl.1, pp. S-15, Japanese

  International conference proceedings


• 膵β細胞不全における転写因子C/EBPβの関与

  KIDO YOSHIAKI

  Jul. 2006, 日本臨床分子医学会43回学術総会プログラム・抄録集, pp. 78-78, Japanese

  International conference proceedings


• Ablation of PDK1 in pancreatic beta cells induces diabetes as a result of loss of beta cell mass

  N Hashimoto, Y Kido, T Uchida, SI Asahara, Y Shigeyama, T Matsuda, A Takeda, D Tsuchihashi, A Nishizawa, W Ogawa, Y Fujimoto, H Okamura, KC Arden, PL Herrera, T Noda, M Kasuga

  May 2006, NATURE GENETICS, 38(5) (5), 589 - 593, English

  Scientific journal


• 膵β細胞不全におけるC/EBPβの役割 遺伝子改変マウスを用いた検討

  KIDO YOSHIAKI

  Apr. 2006, 糖尿病, 49巻, Suppl.1, pp. S265-S265, Japanese

  International conference proceedings


• Ion-solid Interactions at Surfaces in Low and Medium Energy Regimes

  Yoshiaki Kido

  2006, Shinku/Journal of the Vacuum Society of Japan, 49(5) (5), 290 - 297, English

  [Refereed]

  Scientific journal


• 2型糖尿病患者におけるメタボリックシンドローム合併例と非合併例の生活習慣の差異についての検討

  中渡瀬友里, 多留ちえみ, SHIOTANI, Hideyuki, TSUTOU, Akimitsu, KIDO, Yoshiaki, OHHARA, Takeshi, MIYAWAKI, Ikuko

  Sep. 2005, 糖尿病合併症, 19巻, Suppl.1, pp.93-93, Japanese

  Scientific journal


• 膵β細胞特異的PDK1遺伝子欠損マウスの解析

  橋本尚子, KIDO, Yoshiaki, 浅原俊一郎, 茂山豊, 松田友和, 竹田章彦, UCHIDA, Toru, 野田哲生, KASUGA, Masato

  Jul. 2005, 日本臨床分子医学会42回学術総会プログラム・抄録集, pp.93-93, Japanese

  International conference proceedings


• 2型糖尿病患者の食事療法負担感尺度の開発

  多留ちえみ, MIYAWAKI, Ikuko, YADA, Mamiko, MIYATA,Satoshi, KIDO, Yoshiaki, 井上朋子, TANIGUCHI,Hiroshi

  Jun. 2005, 糖尿病, 48巻, 6号, pp.435-442, Japanese

  [Refereed]

  Scientific journal


• 膵β細胞特異的PDK1遺伝子欠損マウスの解析

  橋本尚子, KIDO, Yoshiaki, 松田友和, 浅原俊一郎, 茂山豊, 竹田章彦, UCHIDA, Toru, KASUGA, Masato

  Apr. 2005, 糖尿病, 48巻, Suppl.2, pp.S125-S125, Japanese

  International conference proceedings


• 膵β細胞研究の新展開 糖尿病発症機転における膵β細胞の細胞周期異常

  UCHIDA, Toru, KIDO, Yoshiaki, 橋本尚子, 浅原俊一郎, 茂山豊, 松田友和, 竹田章彦, KASUGA, Masato

  Apr. 2005, 糖尿病, 48巻, Suppl.2, pp.S24-S24, Japanese

  International conference proceedings


• Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice

  T Uchida, T Nakamura, N Hashimoto, T Matsuda, K Kotani, H Sakaue, Y Kido, Y Hayashi, KI Nakayama, MF White, M Kasuga

  Feb. 2005, NATURE MEDICINE, 11(2) (2), 175 - 182, English

  [Refereed]

  Scientific journal


• Protein kinase C alpha is implicated in cholecystokinin-induced activation of 70-kd S6 kinase in AR42J cells

  Y Yutsudo, Y Kido, Y Okabayashi, M Matsumoto, W Ogawa, M Ohba, T Kuroki, M Kasuga

  Jan. 2005, PANCREAS, 30(1) (1), 50 - 53, English

  [Refereed]

  Scientific journal


• PKC lambda regulates glucose-induced insulin secretion through modulation of gene expression in pancreatic beta cells

  N Hashimoto, Y Kido, T Uchida, T Matsuda, K Suzuki, H Inoue, M Matsumoto, W Ogawa, S Maeda, H Fujihara, Y Ueta, Y Uchiyama, K Akimoto, S Ohno, T Noda, M Kasuga

  Jan. 2005, JOURNAL OF CLINICAL INVESTIGATION, 115(1) (1), 138 - 145, English

  [Refereed]

  Scientific journal


• Surface structure and lattice vibrations of MnO(0 0 1) analyzed by high-resolution medium energy ion scattering spectroscopy

  Tetsuaki Okazawa, Yoshiaki Kido

  May 2004, Surface Science, 556(2-3) (2-3), 101 - 108, English

  [Refereed]

  Scientific journal


• 膵β細胞においてPKCλはブドウ糖応答性インスリン分泌にかかわる遺伝子発現を調節する

  橋本尚子, KIDO, Yoshiaki, 松田友和, UCHIDA, Toru, KASUGA, Masato

  Apr. 2004, 糖尿病, 47巻, Suppl.1, pp. S261-S261, Japanese

  International conference proceedings


• Role of STAT-3 in regulation of hepatic gluconeogenic genes and carbohydrate metabolism in vivo

  H Inoue, W Ogawa, M Ozaki, S Haga, M Matsumoto, K Furukawa, N Hashimoto, Y Kido, T Mori, H Sakaue, K Teshigawara, SY Jin, H Iguchi, R Hiramatsu, D LeRoith, K Takeda, S Akira, M Kasuga

  Feb. 2004, NATURE MEDICINE, 10(2) (2), 168 - 174, English

  [Refereed]

  Scientific journal


• A case of acute pancreatitis associated with cationic trypsinogen N29T mutation

  F Ochi, M Fujii, T Sakai, M Sugano, K Oshiro, Y Okabayashi, M Mita, Y Kido

  Aug. 2003, PANCREAS, 27(2) (2), 199 - 201, English

  [Refereed]

  Scientific journal


• Rumpled surface structure and lattice dynamics of NiO(001)

  Tetsuaki Okazawa, Yoshihiro Yagi, Yoshiaki Kido

  May 2003, Physical Review B - Condensed Matter and Materials Physics, 67(19) (19), English

  [Refereed]

  Scientific journal


• 膵β細胞特異的PKCλ遺伝子欠損によるブドウ糖応答性インスリン分泌の低下

  橋本尚子, KIDO, Yoshiaki, 土橋大輔, UCHIDA, Toru, KASUGA, Masato

  Apr. 2003, 糖尿病, 46巻, 臨増, pp. S128-S128, Japanese

  International conference proceedings


• Requirement of autophosphorylated tyrosine 992 of EGF receptor and its docking protein phospholipase C gamma l for membrane ruffle formation

  M Nogami, M Yamazaki, H Watanabe, Y Okabayashi, Y Kido, M Kasuga, T Sasaki, T Maehama, Y Kanaho

  Feb. 2003, FEBS LETTERS, 536(1-3) (1-3), 71 - 76, English

  [Refereed]

  Scientific journal


• Dynamic response of target electrons on elastic scattering cross sections for heavy-ion impact on a high-Z atom

  Yasushi Hoshino, Yoshiaki Kido

  2003, Physical Review A - Atomic, Molecular, and Optical Physics, 68(1) (1), 5, English

  [Refereed]

  Scientific journal


• The forkhead transcription factor Foxo1 links insulin signaling to Pdx1 regulation of pancreatic beta cell growth

  T Kitamura, J Nakae, Y Kitamura, Y Kido, WH Biggs, CVE Wright, MF White, KC Arden, D Accili

  Dec. 2002, JOURNAL OF CLINICAL INVESTIGATION, 110(12) (12), 1839 - 1847, English

  [Refereed]

  Scientific journal


• Defective insulin secretion in pancreatic beta cells lacking type 1 IGF receptor

  SH Xuan, T Kitamura, J Nakae, K Politi, Y Kido, PE Fisher, M Morroni, S Cinti, MF White, PL Herrera, D Accili, A Efstratiadis

  Oct. 2002, JOURNAL OF CLINICAL INVESTIGATION, 110(7) (7), 1011 - 1019, English

  [Refereed]

  Scientific journal


• Effects of mutations in the insulin-like growth factor signaling system on embryonic pancreas development and beta-cell compensation to insulin resistance

  Y Kido, J Nakae, ML Hribal, SH Xuan, A Efstratiadis, D Accili

  Sep. 2002, JOURNAL OF BIOLOGICAL CHEMISTRY, 277(39) (39), 36740 - 36747, English

  [Refereed]

  Scientific journal


• CEACAM1 regulates insulin clearance in liver

  MN Poy, Y Yang, K Rezaei, MA Fernstrom, AD Lee, Y Kido, SK Erickson, SM Najjar

  Mar. 2002, NATURE GENETICS, 30(3) (3), 270 - 276, English

  [Refereed]

  Scientific journal


• Preserved pancreatic beta-cell development and function in mice lacking the insulin receptor-related receptor

  T Kitamura, Y Kido, S Nef, J Merenmies, LF Parada, D Accili

  Aug. 2001, MOLECULAR AND CELLULAR BIOLOGY, 21(16) (16), 5624 - 5630, English

  [Refereed]

  Scientific journal


• Mitogenic and metabolic effects of type IIGF receptor overexpression in insulin receptor-deficient hepatocytes

  JJ Kim, BC Park, Y Kido, D Accili

  Aug. 2001, ENDOCRINOLOGY, 142(8) (8), 3354 - 3360, English

  [Refereed]

  Scientific journal


• Lattice dynamics of RbI(001) surface studied by high-resolution medium energy ion scattering and molecular dynamics simulation

  T. Okazawa, S. Ohno, Y. Hoshino, T. Nishimura, Y. Kido

  Jul. 2001, Nuclear Instruments and Methods in Physics Research, Section B: Beam Interactions with Materials and Atoms, 183(1-2) (1-2), 108 - 115, English

  [Refereed]

  Scientific journal


• Genetic modifiers of the insulin resistance phenotype in mice

  Y Kido, N Philippe, AA Schaffer, D Accili

  Apr. 2000, DIABETES, 49(4) (4), 589 - 596, English

  [Refereed]

  Scientific journal


• Rumpled relaxation of TiC(001) and TaC(001) determined by high-resolution medium-energy ion scattering spectroscopy

  Yoshiaki Kido, Tomoaki Nishimura, Yasushi Hoshino, Shigeki Otani, Ryutaro Souda

  2000, Physical Review B - Condensed Matter and Materials Physics, 61(3) (3), 1748 - 1751, English

  [Refereed]

  Scientific journal


• Tissue-specific insulin resistance in mice with mutations in the insulin receptor, IRS-1, and IRS-2

  Y Kido, DJ Burks, D Withers, JC Bruning, CR Kahn, MF White, D Accili

  Jan. 2000, JOURNAL OF CLINICAL INVESTIGATION, 105(2) (2), 199 - 205, English

  [Refereed]

  Scientific journal


• Expression of kinase-inactive mutant insulin receptors does not rescue insulin receptor-deficient mice from perinatal death

  D Lauro, Y Kido, H Hayashi, Y Ebina, D Accili

  Dec. 1999, DIABETOLOGIA, 42(12) (12), 1441 - 1442, English

  [Refereed]

  Scientific journal


• Differential signaling of insulin and IGF-1 receptors to glycogen synthesis in murine hepatocytes

  BC Park, Y Kido, D Accili

  Jun. 1999, BIOCHEMISTRY, 38(23) (23), 7517 - 7523, English

  [Refereed]

  Scientific journal


• Impaired glucose tolerance in mice with a targeted impairment of insulin action in muscle and adipose tissue

  D Lauro, Y Kido, AL Castle, MJ Zarnowski, H Hayashi, Y Ebina, H Hayashi, D Accili

  Nov. 1998, NATURE GENETICS, 20(3) (3), 294 - 298, English

  [Refereed]

  Scientific journal


• Shc phosphotyrosine-binding domain dominantly interacts with epidermal growth factor receptors and mediates Ras activation in intact cells

  K Sakaguchi, Y Okabayashi, Y Kido, S Kimura, Y Matsumura, K Inushima, M Kasuga

  Apr. 1998, MOLECULAR ENDOCRINOLOGY, 12(4) (4), 536 - 543, English

  [Refereed]

  Scientific journal


• Identification of sirm, a novel insulin-regulated SH3 binding protein that associates with Grb-2 and FYN

  P Salvatore, CR Hanash, Y Kido, Y Imai, D Accili

  Mar. 1998, JOURNAL OF BIOLOGICAL CHEMISTRY, 273(12) (12), 6989 - 6997, English

  [Refereed]

  Scientific journal


• A new toroidal electrostatic analyzer and application to surface analysis

  Tomoaki Nishimura, Atsushi Ikeda, Yoshiaki Kido

  American Institute of Physics Inc., 1998, Review of Scientific Instruments, 69(4) (4), 1671 - 1675, English

  [Refereed]

  Scientific journal


• Enhancement of the mitogenic effect by artificial juxtacrine stimulation using immobilized EGF

  Y Ito, JS Li, T Takahashi, Y Imanishi, Y Okabayashi, Y Kido, M Kasuga

  Mar. 1997, JOURNAL OF BIOCHEMISTRY, 121(3) (3), 514 - 520, English

  [Refereed]

  Scientific journal


• Si-O bond formation by oxygen implantation into silicon

  Kenji Kajiyama, Tomoaki Yoneda, Yuji Fujioka, Yoshiaki Kido

  Elsevier, 1997, Nuclear Instruments and Methods in Physics Research, Section B: Beam Interactions with Materials and Atoms, 121(1-4) (1-4), 315 - 318, English

  [Refereed]

  Scientific journal


• Tryptophan modulates exocrine secretory function in rat pancreatic acini

  T Okutani, Y Okabayashi, M Koide, K Matsushita, M Fujii, H Hasegawa, Y Kido, M Otsuki, M Kasuga

  Apr. 1996, JOURNAL OF GASTROENTEROLOGY, 31(2) (2), 254 - 259, English

  [Refereed]

  Scientific journal


• Interaction of Shc with adaptor protein adaptins

  Y Okabayashi, Y Sugimoto, NF Totty, J Hsuan, Y Kido, K Sakaguchi, Gout, I, MD Waterfield, M Kasuga

  Mar. 1996, JOURNAL OF BIOLOGICAL CHEMISTRY, 271(9) (9), 5265 - 5269, English

  [Refereed]

  Scientific journal


• EGF-INDUCED ACTIVATION OF 70-KDA S6 KINASE IN CHO CELLS EXPRESSING HUMAN EGF RECEPTORS

  Y KIDO, Y OKABAYASHI, T OKUTANI, Y SUGIMOTO, K SAKAGUCHI, M KASUGA

  Apr. 1995, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 209(1) (1), 131 - 138, English

  [Refereed]

  Scientific journal


• Structural analysis of erbium sheet-doped GaAs grown by molecular-beam epitaxy, with ion channeling followed by Monte Carlo simulation

  Jyoji Nakata, Nicolas Jourdan, Hiroshi Yamaguchi, Kenichiro Takahei, Yasuich Yamamoto, Yoshiaki Kido

  1995, Journal of Applied Physics, 77(7) (7), 3095 - 3103, English

  [Refereed]

  Scientific journal


• GRB2/ASH BINDS DIRECTLY TO TYROSINE-1068 AND TYROSINE-1086 AND INDIRECTLY TO TYROSINE-1148 OF ACTIVATED HUMAN EPIDERMAL GROWTH-FACTOR RECEPTORS IN INTACT-CELLS

  T OKUTANI, Y OKABAYASHI, Y KIDO, Y SUGIMOTO, K SAKAGUCHI, K MATUOKA, T TAKENAWA, M KASUGA

  Dec. 1994, JOURNAL OF BIOLOGICAL CHEMISTRY, 269(49) (49), 31310 - 31314, English

  [Refereed]

  Scientific journal


• TYROSINE-1148 AND TYROSINE-1173 OF ACTIVATED HUMAN EPIDERMAL GROWTH-FACTOR RECEPTORS ARE BINDING-SITES OF SHC IN INTACT-CELLS

  Y OKABAYASHI, Y KIDO, T OKUTANI, Y SUGIMOTO, K SAKAGUCHI, M KASUGA

  Jul. 1994, JOURNAL OF BIOLOGICAL CHEMISTRY, 269(28) (28), 18674 - 18678, English

  [Refereed]

  Scientific journal


• EFFECT OF ISLET HORMONES ON SECRETIN-STIMULATED EXOCRINE SECRETION IN ISOLATED-PERFUSED RAT PANCREAS

  H HASEGAWA, Y OKABAYASHI, M KOIDE, Y KIDO, T OKUTANI, K MATSUSHITA, M OTSUKI, M KASUGA

  Jul. 1993, DIGESTIVE DISEASES AND SCIENCES, 38(7) (7), 1278 - 1283, English

  [Refereed]

  Scientific journal


• IN-VITRO INHIBITORY EFFECT OF SOMATOSTATIN ON SECRETIN ACTION IN EXOCRINE PANCREAS OF RATS

  K MATSUSHITA, Y OKABAYASHI, H HASEGAWA, M KOIDE, Y KIDO, T OKUTANI, Y SUGIMOTO, M KASUGA

  Apr. 1993, GASTROENTEROLOGY, 104(4) (4), 1146 - 1152, English

  [Refereed]

  Scientific journal


• Effect of cholecystokinin and secretin on insulin binding to rat pancreatic acini and pancreatic cancer cell line AR42J cells.

  OKABAYASHI Yoshinori, KOIDE Makoto, HASEGAWA Hiroshi, OKUTANI Toshio, KIDO Yoshiaki, MATSUSHITA Kenji, OTSUKI Makoto, KASUGAI Masato

  In order to clarify the interaction of hormones which exert various effects on the exocrine pancreas, we investigated the effect of cholecystokinin (CCK) and secretin on subsequent insulin binding to pancreatic acini and cultured AR42J cells derived from azaserine-induced acinar cell carcinoma of the pancreas. CCK at concentrations of 100pM-lOnM inhibited subsequent ¹²⁵I-insulin binding to pancreatic acini. 12-O-tetradecanoylphorbol 13-acetate (TPA) inhibited ¹²⁵I-insulin binding whereas A23187 had little effect, suggesting that the in-hibitory effect of CCK is mediated by protein kinase C. On the other hand, 100pM-10nM secretin had no effect on subsequent ¹²⁵I-insulin binding to pancreatic acini, although higher concentrations of forskolin and 8 bromoadenosine 3', 5'-cyclic monophosphate inhibited ¹²⁵I-insulin binding. In addition, secretin exerted no potentiating effect on the inhibitory effect of CCK on ¹²⁵I-insulin binding to pancreatic acini. Based on these results, we further investigated the effect of CCK and TPA on subsequent ¹²⁵I-insulin binding to AR42J cells. In this carcinoma cell line, inhibitory effect of CCK and TPA on insulin binding was completely abolished. The present results suggest, therefore, that hormonal interaction may play an important role in the regulation of exocrine pancreatic function including acinar cell growth.

  The Japanese Society of Gastroenterology, 1993, Nippon Shokakibyo Gakkai Zasshi, 90(3) (3), 685 - 692, Japanese


• Inhibitory Effect of Somatostatin Analogue, SMS 201-995, on sEcretin-Stimulatedexocrine Secretion in Isolated Perf Used Rat Pancreas

  Hiroshi Hasegawa, Yoshinori Okabayashi, Makoto Koide, Yoshiaki Kido, Toshio Okutani, Kenji Matsushita, Yutaka Sugimoto, Takahiko Nakamura, Makoto Otsuki, Masato Kasuga

  1993, nippon shokakibyo gakkai zasshi, 90(5) (5), 1425 - 1431, English

  [Refereed]

  Scientific journal


• Plasma Cholecystokinin Levels in Rats with Pancreatic Insufficiency Induced by Intra Ductal Injection of Oleic Acid

  Yoshiaki Kido, Makoto Koide, Satoshi Tani, Yoshinori Okabayashi, Makoto Otsuki

  1993, nippon shokakibyo gakkai zasshi, 90(2) (2), 154 - 158, English

  [Refereed]

  Scientific journal


• Inhibitory effect of somatostatin analog, SMS 201-995, on exocrine secretion from isolated rat pancreatic acini

  Kenji Matsushita, Yoshinori Okabayashi, Takahiko Nakamura, Masatoshi Fujii, Satoshi Tani, Takashi Fujisawa, Makoto Koide, Hiroshi Hasegawa, Yoshiaki Kido, Toshio Okutani, Masato Kasuga

  1992, Nippon Shokakibyo Gakkai Zasshi, 89(6) (6), 1369 - 1374, English

  [Refereed]

  Scientific journal


• Monte Carlo simulation of ion-channeling spectra from partially damaged crystals

  Hirohiko Nakano, Yoshiaki Kido

  1992, Journal of Applied Physics, 71(1) (1), 133 - 139, English

  [Refereed]

  Scientific journal


• Energy straggling for medium-energy H+ beams penetrating Cu, Ag, and Pt

  Yoshiaki Kido, Takanori Koshikawa

  1991, Physical Review A, 44(3) (3), 1759 - 1767, English

  [Refereed]

  Scientific journal


• Dose dependence of surface damage profiles for Ge(111) irradiated with 3 keV Ar+

  Yoshiaki Kido, Hirohiko Nakano

  Dec. 1990, Surface Science, 239(3) (3), 254 - 260, English

  [Refereed]

  Scientific journal


• REGULATORY EFFECT OF CHOLECYSTOKININ ON SUBSEQUENT INSULIN BINDING TO PANCREATIC ACINI

  Y OKABAYASHI, M OTSUKI, T NAKAMURA, M KOIDE, H HASEGAWA, T OKUTANI, Y KIDO

  Apr. 1990, AMERICAN JOURNAL OF PHYSIOLOGY, 258(4) (4), E562 - E568, English

  [Refereed]

  Scientific journal

• 膵β細胞由来エクソソームの臓器連関に関する解析

  井上裕行, 横井愛紗, 後藤綾乃, 篠塚祐奈, 藤井智子, 木戸良明, 淺原俊一郎

  2025, 日本糖尿病・肥満動物学会年次学術集会プログラム・講演抄録集, 38th


• 糖尿病病態における膵β細胞由来エクソソームの動態および役割の解明

  横井愛紗, 淺原俊一郎, 木村真希, 木戸希, 鈴木隆弘, 木戸良明, 小川渉

  2024, 日本内分泌学会雑誌, 100(1) (1)


• 糖尿病病態における膵β細胞由来エクソソームの動態および役割の解明

  横井愛紗, 淺原俊一郎, 木村真希, 鈴木宏隆, 木戸希, 木戸良明, 小川渉

  2024, 日本糖尿病・肥満動物学会年次学術集会プログラム・講演抄録集, 37th


• 2型糖尿病モデルマウスである膵β細胞特異的TSC2ノックアウトマウスの解析

  大中萌, 大中萌, 前野鮎美, 前野鮎美, 木戸希, 清家雅子, 木村真希, 淺原俊一郎, 木戸良明

  2024, 日本分子生物学会年会プログラム・要旨集(Web), 47th


• mTORC1恒常的活性化による膵β細胞量減少機序の検討

  前野鮎美, 前野鮎美, 大中萌, 大中萌, 木戸希, 清家雅子, 木村真希, 淺原俊一郎, 木戸良明

  2024, 日本分子生物学会年会プログラム・要旨集(Web), 47th


• 骨格筋由来エクソソームの動態および糖代謝に及ぼす影響の解析

  鈴木宏隆, 淺原俊一郎, 横井愛紗, 木戸希, 木村真希, 木戸良明, 小川渉

  2024, 糖尿病(Web), 67(Suppl) (Suppl)


• 2型糖尿病の病態把握における肝線維化マーカーFib4indexを用いた検討

  井上裕行, 井上裕行, 淺原俊一郎, 中村文彦, 木戸良明

  2023, 糖尿病(Web), 66(4) (4)


• 糖尿病病態における膵β細胞由来エクソソームの動態および役割の解明

  横井愛紗, 淺原俊一郎, 木村真希, 清家雅子, 鈴木宏隆, 木戸良明, 小川渉

  2023, 糖尿病(Web), 66(Suppl) (Suppl)


• Examination of pancreatic βcell plasticity induced by the activation of mTORC1

  田中ちひろ, 清家雅子, 木村真希, 淺原俊一郎, 木戸良明

  2023, 日本分子生物学会年会プログラム・要旨集(Web), 46th


• 膵β細胞におけるmTORC1活性化は膵外分泌細胞への分化を誘導する

  清家雅子, 淺原俊一郎, 木村真希, 鈴木宏隆, 横井愛紗, 椎木幾久子, 田部勝也, 木戸良明, 木戸良明, 小川渉

  2023, 糖尿病(Web), 66(Suppl) (Suppl)


• Usefulness of the self‐reported Dementia Assessment Sheet for Community‐based Integrated Care System‐21 items (DASC‐21) in the community‐dwelling elderly

  Rei Ono, Kazuaki Uchida, Rika Kawaharada, Yoshiaki Kido, Hisafumi Yasuda, Hisatomo Kowa

  Wiley, Dec. 2020, Alzheimer's & Dementia, 16(S10) (S10)


• mTORC1 Signaling: A Double-Edged Sword in Diabetic β Cells

  ArdestaniA, LupseB, Kido Yoshiaki, LeibowitzG, MaedlerK

  Feb. 2018, Cell Metab, 27(2) (2), 314 - 331, English

  [Refereed]

  Introduction scientific journal


• 糖尿病関連細胞内小器官 小胞体ストレスと膵β細胞

  高井智子, 松田友和, Kido Yoshiaki

  Apr. 2017, Diabetes Frontier, 28(2号) (2号), 193 - 198, Japanese

  Introduction commerce magazine


• 2型糖尿病の病態把握におけるMPV(平均血小板容積)の有用性に関する検討

  井上裕行, 斉藤真裕美, 胡内久美子, 吉村豊, 石田英和, 中谷敏也, 淺原俊一郎, 木戸良明, 木戸良明, 菊池英亮

  2017, 糖尿病(Web), 60(Suppl) (Suppl)


• 海外文献紹介：Perinatal Tolerance to Proinsulin is Sufficient to Prevent Autoimmune Diabetes

  若藤 諒, YASUDA HISAFUMI, 木戸 良明

  Jan. 2017, Diabetes Frontier, 28(1) (1), 114 - 115, Japanese

  [Invited]

  Book review


• 【エピジェネティクスとアンチエイジング】 糖尿病とエピジェネティクス

  淺原俊一郎, Kido Yoshiaki, 脇裕典, 山内敏正, 門脇孝

  Jan. 2017, アンチ・エイジング医学, 12(6号) (6号), 783 - 790, Japanese

  Introduction commerce magazine


• The role of casein kinase 2 in ER stress associated pancreatic beta cell failure

  Yuki Matsuura, Tomoko Takai, Tomokazu Matsuda, Emi Terashi, Ayumi Kanno, Syun-ichiro Asahara, Yoshiaki Kido

  Oct. 2016, DIABETES RESEARCH AND CLINICAL PRACTICE, 120, S42 - S42, English

  Summary international conference


• 【糖尿病の遺伝素因の解明研究】 多遺伝子型(polygenic)糖尿病の解析 アジア人型感受性遺伝子KCNQ1欠損マウスを用いた病態解析

  淺原俊一郎, Kido Yoshiaki

  Aug. 2016, Diabetes Frontier, 27(4号) (4号), 496 - 501, Japanese

  Introduction scientific journal


• 【膵β細胞機能不全のメカニズム】 膵β細胞量の調節因子

  Kido Yoshiaki

  Jun. 2016, 糖尿病, 59(5号) (5号), 326 - 328, Japanese

  Introduction scientific journal


• GCN2, a type 2 diabetes mellitus susceptibility gene, is associated with the regulation of pancreatic beta cell mass

  K. Masuda, A. Kanno, S-I. Asahara, R. Yoshitomi, T. Matsuda, M. Kimura-Koyanagi, Y. Shibutani, N. Yokoi, M. Kasuga, S. Seino, Y. Kido

  Sep. 2015, DIABETOLOGIA, 58, S240 - S240, English

  Summary international conference


• GCN2, a Type 2 Diabetes Mellitus Susceptibility Gene, Is Associated with the Regulation of Pancreatic beta-Cell Mass

  Ayumi Kanno, Katsuhisa Masuda, Shun-Ichiro Asahara, Maki Kimura, Tomokazu Matsuda, Masato Kasuga, Wataru Ogawa, Susumu Seino, Yoshiaki Kido

  Jun. 2015, DIABETES, 64, A599 - A599, English

  Summary international conference


• Reduction in Pancreatic beta-Cell Mass Caused by Enhanced Expression of Cdkn1c via Interaction between C/EBP beta and Epigenetic Control

  Shun-Ichiro Asahara, Yuka Ihara, Hiroyuki Inoue, Kyoko Teruyama, Mizuki Hara, Maki Kimura, Tomokazu Matsuda, Susumu Seino, Yoshiaki Kido

  Jun. 2015, DIABETES, 64, A578 - A578, English

  Summary international conference


• 膵β細胞量の調節因子

  淺原俊一郎, Kido Yoshiaki

  2015, 最新医学, 70, 487 - 495, Japanese

  Introduction commerce magazine


• 膵β細胞のインスリン抵抗性

  淺原俊一郎, Kido Yoshiaki

  2015, Diabetes Frontier, 26, 321 - 325, Japanese

  Introduction commerce magazine


• 膵β細胞におけるmTORC1シグナルとオートファジー

  AlbertoBartolomé, Kido Yoshiaki

  2015, 内分泌・糖尿病・代謝内科, 40, 439 - 444, Japanese

  Introduction commerce magazine


• SU薬

  木村真希, 松田友和, Kido Yoshiaki

  2015, 月刊糖尿病, 7, 88 - 94, Japanese

  Introduction commerce magazine


• Cross-interaction between C/EBPbeta and AMPK determines the pancreatic beta cell mass

  Y. Mieda, T. Matsuda, T. Kawamoto, E. Suzuki, S-I. Asahara, A. Kanno, M. Koyanagi, Y. Kido

  Sep. 2014, DIABETOLOGIA, 57, S191 - S191, English

  Summary international conference


• Reduction in pancreatic beta cell mass caused by enhanced expression of Cdkn1c via interaction between C/EBP beta and epigenetic control

  Y. Ihara, S. -I. Asahara, H. Inoue, K. Teruyama, T. Matsuda, S. Seino, Y. Kido

  Sep. 2014, DIABETOLOGIA, 57, S177 - S177, English

  Summary international conference


• 膵β細胞のKcnq1遺伝子領域におけるエピジェネティクス制御機構の解析

  淺原 俊一郎, 照山 杏子, 伊原 佑香, 井上 裕行, 川田 有希奈, 江藤 博昭, 松田 友和, 春日 雅人, 清野 進, 木戸 良明

  日本臨床分子医学会, Apr. 2014, 日本臨床分子医学会学術総会プログラム・抄録集, 51回, 77 - 77, Japanese


• 膵β細胞における細胞周期調節蛋白p57の機能解析

  原瑞季, 淺原俊一郎, 伊原佑香, 井上裕行, 照山杏子, 松田友和, 木村(小柳)真希, 中山敬一, 木戸良明, 木戸良明

  2014, 日本分子生物学会年会プログラム・要旨集(Web), 37th


• 膵β細胞量調節とエピジェネティクス

  Kido Yoshiaki

  2014, 糖尿病と妊娠, 14, 39 - 43, Japanese

  Introduction commerce magazine


• ERストレスと膵β細胞不全

  松田友和, Kido Yoshiaki

  2014, 内分泌・糖尿病・代謝内科, 38, 312 - 319, Japanese

  Introduction commerce magazine


• Paternal allelic mutation at the Kcnq1 locus reduces pancreatic beta cell mass via epigenetic modification of Cdkn1c

  H. Inoue, S. -I. Asahara, H. Etoh, K. Teruyama, Y. Ihara, T. Matsuda, M. Koyanagi-Kimura, A. Kanno, K. Nagashima, W. Nishimura, K. Yasuda, N. Inagaki, S. Seino, M. Kasuga, Y. Kido

  Sep. 2013, DIABETOLOGIA, 56, S15 - S16, English

  Summary international conference


• Modulation of C/EBP beta expression via AMPK regulates pancreatic beta cell mass

  H. Takahashi, T. Matsuda, Y. Mieda, S. -I. Asahara, E. Terashi, A. Kanno, M. Koyanagi, A. Bartolome, S. Seino, Y. Kido

  Sep. 2013, DIABETOLOGIA, 56, S215 - S215, English

  Summary international conference


• 膵β細胞特異的C/EBPβトランスジェニックマウスに対するビルダグリプチンとメトホルミン併用による膵β細胞保護作用

  高橋宏昌, 松田友和, 三枝祐介, 清水忍, 淺原俊一郎, 小柳真希, 神野歩, 清野進, 木戸良明

  2013, 糖尿病, 56(Supplement 1) (Supplement 1)


• インスリノーマにおけるインスリン分泌特性と遺伝子発現の解析

  小柳真希, 松田友和, 廣田勇士, 橋本尚子, 淺原俊一郎, 中村友昭, 木戸良明, 坂口一彦, 小川渉, 清野進

  2013, 日本内科学会雑誌, 102


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  神野歩, 吉冨理紗, 淺原俊一郎, 松田友和, 小柳真希, 渋谷由紀, 横井伯英, 春日雅人, 清野進, 木戸良明

  2013, 糖尿病, 56(Supplement 1) (Supplement 1)


• DPP4阻害薬MK-626が膵β細胞特異的mTORC1活性亢進モデルマウスに及ぼす影響

  三上智子, 小柳真希, 松田友和, 神野歩, 淺原俊一郎, 春日雅人, 清野進, 木戸良明

  2013, 糖尿病, 56(Supplement 1) (Supplement 1)


• 膵β細胞量の調節因子

  Kido Yoshiaki

  2013, Diabetes Frontier, 24, 507 - 512, Japanese

  Introduction scientific journal


• 糖尿病学の進歩

  Kido Yoshiaki

  2013, 臨床病理, 61, 941 - 947, Japanese

  Introduction scientific journal


• Pancreatic beta cell failure mediated by mTORC1 hyperactivity and autophagic impairment

  A. Bartolome, M. Kimura-Koyanagi, S. Shimizu, A. Kanno, C. Guillen, M. Benito, S. -I. Asahara, Y. Kido

  Oct. 2012, DIABETOLOGIA, 55, S222 - S223, English

  Summary international conference


• Reduction in pancreatic beta cell mass caused by enhanced expression of Cdkn1c as a result of interaction between C/EBP beta and epigenetic control

  K. Teruyama, S. -I. Asahara, H. Inoue, H. Etoh, T. Matsuda, S. Seino, Y. Kido

  Oct. 2012, DIABETOLOGIA, 55, S212 - S212, English

  Summary international conference


• 移植直後の膵島細胞のHMGB1

  Kido Yoshiaki

  Feb. 2012, BIO Clinica, 27巻, 2号, pp. 197-202, Japanese

  Introduction scientific journal


• ER stressと膵β細胞 (糖尿病) -- (基礎分野での進歩)

  松田 友和, 木戸 良明

  中外医学社, 2012, Annual review. 糖尿病・代謝・内分泌, 2012, 10 - 18, Japanese


• 2型糖尿病候補遺伝子Kcnq1遺伝子領域が膵β細胞に及ぼす影響の解析

  井上裕行, 淺原俊一郎, 江藤博昭, 照山杏子, 伊原佑香, 渋谷由紀, 松田友和, 小柳真希, 神野歩, 西村渉, 長嶋一昭, 安田和基, 稲垣暢也, 清野進, 春日雅人, 木戸良明, 木戸良明

  2012, 日本分子生物学会年会プログラム・要旨集(Web), 35th


• 2型糖尿病候補遺伝子Kcnq1遺伝子領域が膵β細胞に及ぼす影響の解析

  淺原俊一郎, 江藤博昭, 照山杏子, 井上裕行, 渋谷由紀, 小柳真希, 松田友和, 長嶋一昭, 西村渉, 安田和基, 稲垣暢也, 清野進, 春日雅人, 木戸良明, 木戸良明

  2012, 日本糖尿病・肥満動物学会年次学術集会プログラム・講演抄録集, 26th


• インスリンシグナルが低出生体重モデルマウスの膵β細胞量調節に与える影響

  吉田有里, 淵田愛, 小柳真希, 淺原俊一郎, 松田友和, 井上妙, 春日雅人, 清野進, 木戸良明

  2012, 糖尿病, 55(Supplement 1) (Supplement 1)


• 胎内環境と2型糖尿病

  Syunichiro Asahara, Kido Yoshiaki

  2012, 最新医学, 67巻, pp. 93-99, Japanese

  Introduction scientific journal


• 移植直後の膵島細胞とHMGB1

  Syunichiro Asahara, Kido Yoshiaki

  2012, BIO Clinica, 27巻, pp. 91-96, Japanese

  Introduction scientific journal


• 【糖尿病とその合併症の成因-最新の知見-】 胎内環境と2型糖尿病

  Kido Yoshiaki

  Jan. 2012, 最新医学, 67巻, 1号, pp. 93-99, Japanese

  Introduction scientific journal


• Effect of DPP-4 inhibitor vildagliptin on pancreatic beta cell failure in beta cell-specific C/EBP beta transgenic mice

  S. Shimizu, T. Hosooka, T. Matsuda, S. I. Asahara, S. Seino, Y. Kido

  Sep. 2011, DIABETOLOGIA, 54, S328 - S328, English

  Summary international conference


• 膵β細胞におけるmTORC1シグナルはミトコンドリア数増加を介してインスリン分泌を亢進させる

  小柳 真希, 淺原 俊一郎, 松田 友和, 茂山 豊, 渋谷 由紀, 神野 歩, 淵田 愛, 小池 正人, 内山 安男, 清野 進, 春日 雅人, 木戸 良明

  (一社)日本内分泌学会, Apr. 2011, 日本内分泌学会雑誌, 87(1) (1), 279 - 279, Japanese


• 膵β細胞におけるcAMP情報伝達系 (糖尿病) -- (基礎分野での進歩)

  木戸 良明, 柴崎 忠雄, 清野 進

  中外医学社, 2011, Annual review. 糖尿病・代謝・内分泌, 2011, 12 - 19, Japanese


• 2型糖尿病候補遺伝子KCNQ1の膵β細胞に及ぼす役割の検討

  江藤博昭, 淺原俊一郎, 照山杏子, 小柳真希, 渋谷由紀, 松田友和, 長嶋一昭, 西村渉, 安田和基, 清野進, 春日雅人, 木戸良明, 木戸良明

  2011, 日本内分泌学会雑誌, 87(1) (1)


• 低出生体重モデルマウスにおける膵β細胞量調節機構の検討

  吉田有里, 淵田愛, 小柳真希, 淺原俊一郎, 井上妙, 春日雅人, 清野進, 木戸良明, 木戸良明

  2011, 日本分子生物学会年会プログラム・要旨集(Web), 34th


• 低出生体重モデルマウスにおける膵β細胞量調節機構の検討

  吉田有里, 淵田愛, 小柳真希, 淺原俊一郎, 松田友和, 春日雅人, 清野進, 木戸良明, 木戸良明

  2011, 肥満研究, 17(Supplement) (Supplement)


• 2型糖尿病候補遺伝子Kcnq1遺伝子領域が膵β細胞に及ぼす影響の解析

  淺原俊一郎, 江藤博昭, 照山杏子, 小柳真希, 渋谷由紀, 松田友和, 長嶋一昭, 西村渉, 安田和基, 清野進, 春日雅人, 木戸良明

  2011, 糖尿病, 54(Supplement 1) (Supplement 1)


• 膵β細胞特異的C/EBPβトランスジェニックマウスを用いた膵β細胞不全に対するDPP-4阻害剤(ビルダグリプチン)の効果の検討

  清水忍, 細岡哲也, 松田友和, 淺原俊一郎, 小柳真希, 清野進, 木戸良明

  2011, 糖尿病, 54(Supplement 1) (Supplement 1)


• 低出生体重モデルマウスにおける膵β細胞量調節機構の検討

  淵田愛, 吉田有里, 小柳真希, 淺原俊一郎, 松田友和, 井上妙, 春日雅人, 清野進, 木戸良明

  2011, 糖尿病, 54(Supplement 1) (Supplement 1)


• 膵β細胞におけるelF2αキナーゼGCN2の機能解析

  神野歩, 吉冨理紗, 淺原俊一郎, 松田友和, 小柳真希, 渋谷由紀, 春日雅人, 清野進, 木戸良明

  2011, 糖尿病, 54(Supplement 1) (Supplement 1)


• 膵β細胞でのインスリン作用とその障害

  Maki Koyanagi, Kido Yoshiaki

  2011, ホルモンと臨床, 58巻, pp. 43-51, Japanese

  Introduction scientific journal


• Ablation of TSC2 Enhances Mitochondrial Function Via Activation of mTORC1 in beta Cells

  Maki Koyanagi, Yoshiaki Kido, Shun-Ichiro Asahara, Yutaka Shigeyama, Tomokazu Matsuda, Yuki Shibutani, Megumi Fuchita, Tetsuo Noda, Susumu Seino, Masato Kasuga

  Jun. 2010, DIABETES, 59, A91 - A91, English

  Summary international conference


• 膵β細胞におけるmTORシグナルとミトコンドリア機能の検討

  小柳 真希, 木戸 良明, 浅原 俊一郎, 茂山 豊, 松田 友和, 渋谷 由紀, 淵田 愛, 小池 正人, 内山 安男, 春日 雅人, 清野 進

  (一社)日本糖尿病学会, Apr. 2010, 糖尿病, 53(Suppl.1) (Suppl.1), S - 156, Japanese


• Rac1 regulates glucose-induced insulin secretion through the modulation of cytoskeletal organization in beta cells

  Shun-ichiro Asahara, Yoshiaki Kido, Tomokazu Matsuda, Yuki Shibutani, Maki Koyanagi, Susumu Seino, Masato Kasuga

  Mar. 2010, ENDOCRINE JOURNAL, 57, S386 - S386, English

  Summary international conference


• 2型糖尿病候補遺伝子KCNQ1の膵β細胞に及ぼす役割の検討

  江藤博昭, 木戸良明, 木戸良明, 淺原俊一郎, 小柳真希, 渋谷由紀, 松田友和, 清野進, 春日雅人

  2010, 糖尿病, 53(Supplement 1) (Supplement 1)


• 2型糖尿病候補遺伝子KCNQ1の膵β細胞に及ぼす役割の検討

  江藤博昭, 淺原俊一郎, 渋谷由紀, 小柳真希, 照山杏子, 荒木沙織, 清野進, 春日雅人, 木戸良明, 木戸良明

  2010, 生化学


• 【膵β細胞増殖を調節するシグナル】 インスリンシグナル PDK1/TSC2

  Kido Yoshiaki

  Jan. 2010, 内分泌・糖尿病・代謝内科, 30巻, 1, pp. 15-24, Japanese

  Introduction scientific journal


• 膵β細胞における低分子量Gタンパク質Rac1の機能解析 (助成研究報告)

  木戸 良明, 淺原 俊一郎

  神戸大学, Aug. 2009, 神戸大学医学部神緑会学術誌, 25, 64 - 65, Japanese


• Involvement of epigenetics in diabetes mellitus

  浅原 俊一郎, 木戸 良明

  メディカルレビュー社, Jun. 2009, Genome medicine, 9(2) (2), 127 - 131, Japanese


• Effect of the Constitutive Activation of mTORC1 on Mitochondrial Function in Pancreatic beta Cells

  Maki Koyanagi, Yoshiaki Kido, Shun-Ichiro Asahara, Yutaka Shigeyama, Tomokazu Matsuda, Akihiko Takeda, Tae Inoue, Yuki Shibutani, Tohru Uchida, Susumu Seino, Masato Kasuga

  Jun. 2009, DIABETES, 58, A2 - A2, English

  Summary international conference


• 【インスリン作用の原点】 膵β細胞におけるインスリン作用

  Kido Yoshiaki

  May 2009, 糖尿病, 52巻, 5号, pp. 329-331, Japanese

  Introduction scientific journal


• 膵β細胞における低分子量GタンパクRac1の機能解析

  淺原俊一郎, 木戸良明, 橋本尚子, 茂山豊, 松田友和, 竹田章彦, 井上妙, 渋谷由紀, 小柳真希, 内田亨, 春日雅人

  2009, 日本内分泌学会雑誌, 85(1) (1)


• 2型糖尿病候補遺伝子KCNQ1の膵β細胞に及ぼす役割の検討

  渋谷由紀, 木戸良明, 淺原俊一郎, 松田友和, 竹田章彦, 井上妙, 小柳真希, 長嶋一昭, 清野進, 春日雅人

  2009, 糖尿病, 52(Supplement 1) (Supplement 1)


• Rac1 regulates glucose-induced insulin secretion through modulation of cytoskeletal organization in beta cells

  Shun-Ichiro Asahara, Yoshiaki Kido, Yutaka Shigeyama, Tomokazu Matsuda, Akihiko Takeda, Tae Inoue, Yuki Shibutani, Maki Koyanagi, Tohru Uchida, Masato Kasuga

  Jun. 2008, DIABETES, 57, A55 - A55, English

  Summary international conference


• Mechanism for regulation of pancreatic β cell mass

  木戸 良明, 松田 友和

  日本臨床社, May 2008, Japanese journal of clinical medicine, 66, 119 - 123, Japanese


• mTORシグナルによる膵β細胞数・サイズ調節機構の解明

  小柳真希, 木戸良明, 茂山豊, 中野尚子, 浅原俊一郎, 松田友和, 竹田章彦, 井上妙, 渋谷由紀, 内田亨, 野田哲生, 春日雅人

  2008, 糖尿病, 51(Supplement 1) (Supplement 1)


• 膵β細胞における低分子量GタンパクRac1の機能解析

  浅原俊一郎, 木戸良明, 中野尚子, 茂山豊, 松田友和, 竹田章彦, 井上妙, 渋谷由紀, 小柳真希, 内田亨, 春日雅人

  2008, 糖尿病, 51(Supplement 1) (Supplement 1)


• mTORをめぐるシグナルタンパク TSC2ノックアウトマウス

  小柳真希, 木戸良明, 春日雅人

  2008, 生体の科学, 59(6) (6)


• Accumulation of C/EBP beta induces pancreatic beta cell failure by reducing the endoplasmic reticulum function

  Tomokazu Matsuda, Yoshiaki Kido, Naoko Hashimoto, Shun-Ichiro Asahara, Yutaka Shigeyama, Akihiko Takeda, Tae Inoue, Yuki Shibutani, Tohru Uchida, Masato Kasuga

  Jun. 2007, DIABETES, 56, A411 - A411, English

  Summary international conference


• Role of TSC2 in the regulation of pancreatic beta cell mass

  Yutaka Shigeyama, Yoshiaki Kido, Naoko Hashimoto, Shun-Ichiro Asahara, Tomokazu Matsuda, Akihiko Takeda, Tae Inoue, Yuki Shibutani, Tohru Uchida, Tetsuo Noda, Masato Kasuga

  Jun. 2007, DIABETES, 56, A422 - A422, English

  Summary international conference


• 糖尿病発症の分子機構 膵β細胞におけるインスリンシグナリング

  KIDO YOSHIAKI

  Apr. 2007, 分子糖尿病学の進歩: 基礎から臨床まで, 2007巻, pp. 60-65, Japanese

  Introduction scientific journal


• インスリンシグナルと膵β細胞量

  Kido Yoshiaki

  2007, 糖尿病学2007, 巻, , pp. 55-62, Japanese

  Introduction scientific journal


• インスリン分泌の分子機構 膵β細胞の細胞周期異常

  KIDO YOSHIAKI

  Mar. 2006, 分子糖尿病学の進歩: 基礎から臨床まで, pp. 18-25, Japanese

  Introduction scientific journal


• 【シグナル伝達研究2005-'06 生命現象や疾患を支配する分子メカニズムと新しい研究法 現在と未来】 シグナル伝達の異常による疾患・臨床応用 糖尿病とインスリンシグナリング

  KIDO, Yoshiaki, UCHIDA, Toru, OGAWA, Wataru, KASUGA, Masato

  Jun. 2005, 実験医学, 23巻, 11号, pp.1818-1822, Japanese

  Introduction scientific journal


• 【糖・脂質代謝と臓器相関】 膵内外分泌相関と糖脂質代謝

  KIDO, Yoshiaki, 岡林克典

  Nov. 2003, 内分泌・糖尿病科, 17巻, 5号, pp. 427-433, Japanese

  Introduction scientific journal


• Defective glucose-induced insulin secretion in pancreatic beta-cell specific PKC lambda knockout mice

  N Hashimoto, Y Kido, D Tsuchihashi, T Uchida, S Ohno, T Noda, M Kasuga

  Jun. 2003, DIABETES, 52, A3 - A4, English

  Summary international conference


• Charge exchange for medium energy He and Ne ions in a large-angle collision at solid surfaces

  Yoshiaki Kido, Syohei Semba, Yasushi Hoshino

  Feb. 2003, Current Applied Physics, 3(1) (1), 3 - 7, English

  Book review


• Distinct and overlapping functions of insulin and IGF-I receptors

  J Nakae, Y Kido, D Accili

  Dec. 2001, ENDOCRINE REVIEWS, 22(6) (6), 818 - 835, English

  Book review


• Clinical review 125 - The insulin receptor and its cellular targets

  Y Kido, J Nakae, D Accili

  Mar. 2001, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 86(3) (3), 972 - 979, English

  Book review


• Tissue-specific insulin resistance in type 2 diabetes: lessons from gene-targeted mice

  J Nakae, Y Kido, D Accili

  Feb. 2001, ANNALS OF MEDICINE, 33(1) (1), 22 - 27, English

  Book review


• PANC-1細胞の増殖と抗アポトーシスにおけるAktの役割

  よう さん, 岡林克典, 湯通堂仁大, 北村忠弘, 小川渉, 木戸良明, 春日雅人

  2001, 膵臓, 16(3) (3)


• Beta cell development in mice lacking insulin and type 1 IGF receptors

  Y Kido, J Nakae, SH Xuan, A Efstratiadis, D Accili

  May 2000, DIABETES, 49, A256 - A256, English

  Summary international conference


• Identification of differentially expressed cDNAs in muscle of insulin-resistant mice

  H Kanno, J Nakae, Y Kido

  1999, DIABETES, 48, A189 - A189, English

  Summary international conference


• Impaired insulin clearance from the blood of mice with liver-targeted overexpression of a phosphorylation-defective isoform of pp120, a substrate of the receptor tyrosine kinase in the hepatocyte

  SM Najjar, MN Poy, MA Fernstrom, KA Al-Hosaini, Y Kido

  1999, DIABETES, 48, A227 - A227, English

  Summary international conference


• Transgenic knock-out mice with a targeted impairment of insulin action in skeletal muscle and adipose tissue

  D Lauro, Y Kido, H Hayashi, Y Ebina, D Accili

  May 1998, DIABETES, 47, A45 - A45, English

  Summary international conference


• The susceptibility to diabetes in mice carrying a null allele of the insulin receptor gene is genetically determined

  Y Kido, D Accili

  May 1998, DIABETES, 47, A178 - A178, English

  Summary international conference


• EFFECT OF INSULIN ON SECRETIN POTENTIATION OF EXOCRINE SECRETION IN ISOLATED PANCREATIC ACINI

  K MATSUSHITA, Y OKABAYASHI, M KOIDE, H HASEGAWA, Y KIDO, T OKUTANI, Y SUGIMOTO, M KASUGA

  Apr. 1993, GASTROENTEROLOGY, 104(4) (4), A322 - A322, English

  Summary international conference

• 糖尿病2016 / Kcnq1遺伝子領域による膵β細胞量調節機構

  淺原俊一郎, Kido Yoshiaki

  Others, 診断と治療社, 2016, Japanese

  Scholarly book


• アジアにおける国際保健 / アジアにおける糖尿病

  Kido Yoshiaki

  Others, 神戸大学国際保健教育研究センター, 2012, Japanese

  General book


• Annual Review 糖尿病・代謝・内分泌 / ER stress と膵β細胞

  松田 友和, Kido Yoshiaki

  Others, 中外医学社, 2012, Japanese

  General book


• 糖尿病学2011 / 膵β細胞における小胞体ストレスの役割

  松田 友和, Kido Yoshiaki

  Joint work, 診断と治療社, 2011, Japanese

  General book


• Annual Review 糖尿病・代謝・内分泌 / 膵β細胞におけるcAMP情報伝達系

  Kido Yoshiaki, 柴崎 忠雄, 清野 進

  Joint work, 中外医学社, 2011, Japanese

  General book


• 糖尿病ナビゲーター / 膵β細胞の増殖機構

  Kido Yoshiaki

  Others, メディカルビュー社, 2010, Japanese

  Scholarly book


• 糖尿病学の進歩2009 / β細胞のインスリンシグナル

  Kido Yoshiaki

  Joint work, 診断と治療社, 2009, Japanese

  Scholarly book


• よくわかる糖尿病 最新医療 (家庭の医学シリーズ) / 糖尿病の種類

  Kido Yoshiaki

  Joint work, 廣済堂出版, 2009, Japanese

  General book


• 2型糖尿病における膵β細胞研究の進歩 / 糖尿病発症における膵β細胞量の異常

  Kido Yoshiaki

  Joint work, 診断と治療社, 2008, Japanese

  Scholarly book


• 分子糖尿病学の進歩 / 膵細胞におけるインスリンシグナリング

  KIDO, Yoshiaki, 松田 友和

  Joint work, 金原出版, 2007, Japanese

  Scholarly book


• 糖尿病学2007 / インスリンシグナルと膵β細胞量

  Kido Yoshiaki, 竹田 章彦, 中野 尚子, 春日 雅人

  Joint work, 診断と治療社, 2007, Japanese

  General book


• 糖尿病ナビゲーター / 膵細胞の増殖機構

  松田 友和, KIDO, Yoshiaki

  Joint work, メディカルビュー社, 2007, Japanese

  Scholarly book


• 分子糖尿病学の進歩 / 膵細胞の細胞周期異常

  橋本 尚子, 内田 亨, KIDO, Yoshiaki

  Joint work, 金原出版, 2006, Japanese

  Scholarly book


• 分子糖尿病学の進歩 / 膵β細胞の細胞周期異常

  内田亨, Kido Yoshiaki

  Others, 金原出版, 2006, Japanese

  Scholarly book


• 実験医学増刊 シグナル伝達研究2005-’06 / 糖尿病とインスリンシグナリング

  KIDO, Yoshiaki, 内田 亨, 小川 渉, 春日 雅人

  Joint work, 羊土社, 2005, Japanese

  Scholarly book


• 糖尿病 / 膵β細胞におけるインスリンシグナリング

  KIDO, Yoshiaki

  Joint work, 文光堂, 2004, Japanese

  Scholarly book


• KEY WORD 糖尿病 第２版 / プロインスリン変換酵素（PC2,PC3)

  橋本 尚子, KIDO, Yoshiaki

  Joint work, 先端医学社, 2004, Japanese

  Scholarly book


• 看護のための最新医学講座 第31巻 医学と分子生物学 / 代謝・内分泌疾患 糖尿病 膵Ｂ細胞

  Kido Yoshiaki

  Joint work, 中山書店, 2003, Japanese

  Scholarly book


• 分子糖尿病学の進歩 / 個体におけるインスリン作用の解析―トランスジェニックマウスとノックアウトマウス―

  KIDO, Yoshiaki, Domenico Accili

  Joint work, 金原出版, 2000, Japanese

  Scholarly book


• Advances in Molecular and Cellular Endocrinology Vol.13 / Targeted mutations in the insulin signaling unravel the genetics of diabetes mellitus and growth in mice.

  Accili D, KIDO, Yoshiaki

  Joint work, JAI Press Inc., 1999, English

  Scholarly book


• 実験医学増刊 GTP結合蛋白質 / 培養細胞におけるダイナミンとシグナル伝達

  KIDO, Yoshiaki, 岡林 克典, 春日 雅人

  Joint work, 羊土社, 1996, Japanese

  Scholarly book

• Regulation of pancreatic beta cell mass from the interaction of gene-environmental factors

  KIDO Yoshiaki

  International Congres of Diabetes and Metabolism 2019, Oct. 2019, English, International conference

  [Invited]

  Nominated symposium


• SGLT2欠損マウスにおける低炭水化物食摂取が耐糖能、血糖調節ホルモンおよび臓器代謝に及ぼす影響の解明

  韓 桂栄, 浜本 芳之, YOKOI NORIHIDE, KIDO YOSHIAKI, 清野 裕, SEINO SUSUMU

  第22回日本病態栄養学会年次学術集会, Jan. 2019, Japanese, 横浜, 【目的】SGLT2阻害薬は尿糖排泄促進により血糖降下作用を発揮するが、低炭水化物食と併用した際の影響は不明である。そこで、SGLT2阻害状態における低炭水化物摂取が耐糖能、血糖調節ホルモンおよび臓器代謝に与える影響を検討した。【方法】SGLT2変異を有するSAMP10マウス（KO）と野生型のSAMP10（WT）を用いて、通常食（SC）あるいは低炭水化物食（LC）を8週齢から4週間給餌し、血糖・体重変化、経口ブドウ糖負荷試験（OGTT）および腹腔内インスリン負荷試験（IPITT）時の血糖および血糖調節ホルモンを測定した。また、臓器のメタボローム解析、糖代謝関連遺伝子発現解析を行った。【結果】自由摂餌下では両群ともLCで摂取エネルギーがSCより多く体重が増加した。LCではWT群は耐糖能が悪化したのに対し、KO群は悪化しなかった。その際、インスリンおよびG, Domestic conference

  Oral presentation


• 膵β細胞特異的PDK1ノックアウトマウスにおける前糖尿病状態の解析

  土屋 匠子, ASAHARA SHUNICHIROU, 河村 真緒, 林田 彩花, KIDO YOSHIAKI

  日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞特異的PDK1ノックアウトマウスにおける前糖尿病状態の解析

  土屋 匠子, ASAHARA SHUNICHIROU, 河村 真緒, 林田 彩花, KIDO YOSHIAKI

  第41回日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞特異的PDK1ノックアウトマウスにおける血糖値推移とβ細胞量の検討

  伊東 春香, ASAHARA SHUNICHIROU, 原 千佐子, KIMURA MAKI, 神野 歩, 高井 智子, KIDO YOSHIAKI

  日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞特異的PDK1ノックアウトマウスにおける血糖値推移とβ細胞量の検討

  伊東 春香, ASAHARA SHUNICHIROU, 原 千佐子, KIMURA MAKI, 神野 歩, 高井 智子, KIDO YOSHIAKI

  第41回日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞の小胞体ストレス誘導性アポトーシスにおけるCK2の役割

  井上 佳歩, 高井 智子, 松田 友和, 鈴木 江美, 神野 歩, KIMURA MAKI, ASAHARA SHUNICHIROU, KIDO YOSHIAKI

  日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞の小胞体ストレス誘導性アポトーシスにおけるCK2の役割

  井上 佳歩, 高井 智子, 松田 友和, 鈴木 江美, 神野 歩, KIMURA MAKI, ASAHARA SHUNICHIROU, KIDO YOSHIAKI

  第41回日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞のUnfolded Protein ResponseにおけるCK2の役割

  高井 智子, 松田 友和, 井上 佳歩, 鈴木 江美, 神野 歩, KIMURA MAKI, ASAHARA SHUNICHIROU, KIDO YOSHIAKI

  日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞のUnfolded Protein ResponseにおけるCK2の役割

  高井 智子, 松田 友和, 井上 佳歩, 鈴木 江美, 神野 歩, KIMURA MAKI, ASAHARA SHUNICHIROU, KIDO YOSHIAKI

  第41回日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞におけるGCN2/asparaginase/ｍTORC1シグナルの同定

  工藤 倫代, 神野 歩, ASAHARA SHUNICHIROU, 松田 友和, KIMURA MAKI, KIDO YOSHIAKI

  日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 膵β細胞におけるGCN2/asparaginase/ｍTORC1シグナルの同定

  工藤 倫代, 神野 歩, ASAHARA SHUNICHIROU, 松田 友和, KIMURA MAKI, KIDO YOSHIAKI

  第41回日本分子生物学会年会, Nov. 2018, Japanese, 横浜, Domestic conference

  Poster presentation


• 地域在住高齢者の認知機能に対する複合課題プログラム効果の検証

  小野 玲, 古和久朋, 村田峻輔, 安田尚史, 種村留美, KIDO YOSHIAKI

  日本認知症予防学会学術集会, Sep. 2018, Japanese, 東京, Domestic conference

  Oral presentation


• 地域在住高齢者の認知機能に対する複合課題プログラム効果の検証

  ONO REI, 古和 久明, 村田峻輔, YASUDA HISAFUMI, TANEMURA RUMI, KIDO YOSHIAKI

  第8回日本認知症予防学会学術集会, Sep. 2018, Japanese, Domestic conference

  Oral presentation


• Establishment of novel biomarkers for type 2 diabetes using T2DM model mice (2型糖尿病モデルマウスにおける早期診断のためのバイオマーカーの探索)

  河村 真緒, ASAHARA SHUNICHIROU, 土屋 匠子, 林田 彩花, KIDO YOSHIAKI

  日本細胞外小胞学会, Aug. 2018, Japanese, 広島, Domestic conference

  Oral presentation


• Establishment of novel biomarkers for type 2 diabetes using T2DM model mice (2型糖尿病モデルマウスにおける早期診断のためのバイオマーカーの探索)

  河村 真緒, ASAHARA SHUNICHIROU, 土屋 匠子, 林田 彩花, KIDO YOSHIAKI

  第5回日本細胞外小胞学会, Aug. 2018, Japanese, 広島, Domestic conference

  Oral presentation


• SGLT2阻害状態における低炭水化物食摂取が耐糖能、血糖調節ホルモンおよび臓器代謝に及ぼす影響の解明 -SGLT2変異SAMP10マウスを用いた検討-

  韓 桂栄, 浜本 芳之, YOKOI NORIHIDE, 髙木 貞明, 細川 昌則, KIDO YOSHIAKI, 清野 裕, SEINO SUSUMU

  第33回老化促進モデルマウス(SAM)学会学術大会, Jul. 2018, Japanese, 静岡, 【目的】SGLT2阻害薬は尿糖排泄促進により血糖降下作用を発揮するが、低炭水化物食と併用した際の影響は不明である。そこで、SGLT2阻害状態における低炭水化物摂取が耐糖能、血糖調節ホルモンおよび臓器代謝に与える影響を検討した。【方法】SGLT2変異を有するSAMP10マウス（KO）と野生型のSAMP10（WT）を用いて、通常食（SC）あるいは低炭水化物食（LC）を8週齢から4週間給餌し、血糖・体重変化、経口ブドウ糖負荷試験（OGTT）および腹腔内インスリン負荷試験（IPITT）時の血糖および血糖調節ホルモンを測定した。また、臓器のメタボローム解析、糖代謝関連遺伝子発現解析を行った。【結果】自由摂餌下では両群ともLCで摂取エネルギーがSCより多く体重が増加した。LCではWT群は耐糖能が悪化したのに対し、KO群は悪化しなかった。その際、インスリンおよびG, Domestic conference

  Oral presentation


• ヒトips細胞を用いた膵内分泌細胞への分化誘導

  山田 瑞姫, ASAHARA SHUNICHIROU, 遠山 春希, 下野 名奈子, 原 瑞希, 田中 孝一, 松田 友和, KIMURA MAKI, 神野 歩, 高井 智子, 鈴木 江美, AOI TAKASHI, KIDO YOSHIAKI

  第61回日本糖尿病学会年次学術集会, May 2018, Japanese, 東京, Domestic conference

  Others


• グルタミン-グルタミン酸シグナルによるインスリン分泌増強機構の解明

  韓 桂栄, YOKOI NORIHIDE, グプルジャン ゲニ, 村尾 直哉, TAKAHASHI HARUMI, 清野 裕, KIDO YOSHIAKI, SEINO SUSUMU

  第61回日本糖尿病学会年次学術集会, May 2018, Japanese, 東京, 【目的】膵β細胞におけるグルタミン-グルタミン酸シグナルによるインクレチン応答性インスリン分泌（IIIS）増強機構を解明する。【方法】インクレチン応答性膵β細胞株（MIN6-K8）、リンゴ酸-アスパラギン酸シャトル酵素の欠損株（AST1-KO）、小胞型グルタミン酸トランスポーターの欠損株（VGLUTs-KO）、グルタミン酸合成酵素であるグルタミナーゼの阻害剤（BPTES）を用いてインスリン分泌におけるグルタミン処置の効果を検討した。【結果】AST1-KOではIIISが障害されていたが、グルタミン処置により回復した。一方、VGLUTs-KOにおけるIIISの障害はグルタミン処置により回復しなかった。また、グルタミンによるインスリン分泌増強効果はBPTESにより消失した。【結語】グルタミンはグルタミナーゼによりグルタミン酸に変換され、VGLUTsを介して, Domestic conference

  Oral presentation


• 2型糖尿病感受性遺伝子GCN2はSestrin2を介して膵β細胞量の調節に関与する

  古林 鮎子, 神野 歩, ASAHARA SHUNICHIROU, 松田 友和, KIMURA MAKI, KIDO YOSHIAKI

  日本内分泌学会, Apr. 2018, Japanese, 宮崎, Domestic conference

  Oral presentation


• 2型糖尿病感受性遺伝子GCN2はSestrin2を介して膵β細胞量の調節に関与する

  古林 鮎子, 神野 歩, ASAHARA SHUNICHIROU, 松田 友和, KIMURA MAKI, KIDO YOSHIAKI

  第91回日本内分泌学会学術総会, Apr. 2018, Japanese, 宮崎, Domestic conference

  Oral presentation


• 金属アレルギー患者に対する管理栄養士による栄養指導の有効性と尿中金属濃度

  三ヶ尻 礼子, Fukunaga Atsushi, 三好 真琴, 前重 伯壮, 吉岡 愛育, Washio Ken, 正木 太朗, 山本 育子, Takahashi Michiko, Ogawa Wataru, Kido Yoshiaki, Nishigori Chikako, 宇佐美 眞

  第33回日本静脈経腸栄養学会学術集会（実験研究助成金受賞者講演）, Feb. 2018, Japanese, 日本静脈経腸栄養学会, 横浜, Domestic conference

  Keynote oral presentation


• SGLT2欠損モデルにおける摂取炭水化物量がインスリン・グルカゴン・GIPに及ぼす影響の検討

  韓 桂栄, 浜本 芳之, Yokoi Norihide, Kido Yoshiaki, 清野 裕, Seino Susumu

  第21回日本病態栄養学会年次学術集会, Jan. 2018, Japanese, 日本病態栄養学会, 京都, Domestic conference

  Oral presentation


• 膵β細胞の小胞体ストレス誘導性アポトーシスにおけるCK2βの役割

  井上 佳歩, 高井 智子, 松田 友和, 鈴木 江美, 神野 歩, KIMURA MAKI, ASAHARA SHUNICHIROU, KIDO YOSHIAKI

  第40回日本分子生物学会年会, Dec. 2017, Japanese, 神戸, Domestic conference

  Oral presentation


• 高脂肪食負荷GCN2欠損マウスの膵島におけるmTORC1シグナル調節機構の解明

  古林 鮎子, 神野 歩, 増田 勝久, 吉富 理紗, KIMURA MAKI, 松田 友和, ASAHARA SHUNICHIROU, KIDO YOSHIAKI

  第40回日本分子生物学会年会, Dec. 2017, Japanese, 神戸, Domestic conference

  Oral presentation


• ヒトiPS細胞を用いた膵内分泌細胞への分化誘導法の確立

  山田 瑞姫, ASAHARA SHUNICHIROU, 下野 名奈子, 田中 孝一, 松田 友和, KIMURA MAKI, 神野 歩, 高井 智子, 鈴木 江美, AOI TAKASHI, KIDO YOSHIAKI

  第40回日本分子生物学会年会, Dec. 2017, Japanese, 神戸, Domestic conference

  Poster presentation


• P-0503 Effect of removal of glucotoxicity by SGLT2 inhibitor dapagliflozin on the gene expression in pancreatic beta cells

  ASAHARA SHUNICHIROU, 大橋, KIDO YOSHIAKI

  International Diabetes Federation, Dec. 2017, English, Abu Dhabi, International conference

  Poster presentation


• Beta cell mass

  KIDO YOSHIAKI

  International Diabetes Federation, Dec. 2017, English, Abu Dhabi, International conference

  [Invited]

  Nominated symposium


• 2型糖尿病感受性遺伝子による膵β細胞量調節機構

  KIDO YOSHIAKI

  新学術創成研究機構 革新的統合バイオ研究コア 栄養・代謝研究ユニットセミナー, Dec. 2017, Japanese, 金沢, Domestic conference

  [Invited]

  Invited oral presentation


• 2型糖尿病感受性遺伝子Kcnq1による膵β細胞量調節機構

  KIDO YOSHIAKI

  2017年度遺伝研研究会「マウスとラットで拓く新しい比較実験動物学」, Dec. 2017, Japanese, 三島, Domestic conference

  [Invited]

  Invited oral presentation


• 2型糖尿病モデルマウスにおける新規バイオマーカーの探索

  河村 真緒, 土屋 匠子, ASAHARA SHUNICHIROU, KIDO YOSHIAKI

  第40回日本分子生物学会年会, Dec. 2017, Japanese, 神戸, Domestic conference

  Oral presentation


• Analysis of Pathogenic Mechanism by Susceptibility Genes of T2DM Using Human iPS Cells

  ASAHARA SHUNICHIROU, KIDO YOSHIAKI

  77th Scientific Sessions of American Diabetes Association, Jun. 2017, English, San Diego, International conference

  Poster presentation


• 膵β細胞の小胞体ストレス誘導性アポトーシスにおけるCK2βの役割

  高井 智子, 松田 友和, 井上 佳歩, 松浦 有希, 鈴木 江美, 神野 歩, KIMURA MAKI, ASAHARA SHUNICHIROU, OGAWA WATARU, KIDO YOSHIAKI

  第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

  Oral presentation


• 脂肪酸が膵β細胞の小胞体に及ぼす影響

  鈴木 江美, 松田 友和, 川本 剛士, 松浦 有希, 高井 智子, 神野 歩, KIMURA MAKI, ASAHARA SHUNICHIROU, OGAWA WATARU, KIDO YOSHIAKI

  第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

  Poster presentation


• ヒトIps細胞を用いた2型糖尿病発症機序の解明

  下野 名奈子, ASAHARA SHUNICHIROU, 原 瑞季, 田中 孝一, 松田 友和, KIMURA MAKI, 神野 歩, 高井 智子, 鈴木 江美, AOI TAKASHI, KIDO YOSHIAKI

  第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

  Poster presentation


• Regulation of pancreatic beta cell mass from the interaction of geneenvironment factors

  KIDO YOSHIAKI

  9th AASD Scientific Meeting, May 2017, English, NAGOYA, International conference

  [Invited]

  Nominated symposium


• Regulation of pancreatic beta cell mass from the interaction of geneenvironment factors

  KIDO YOSHIAKI

  第60回日本糖尿病学会年次学術集会, May 2017, English, 名古屋, Domestic conference

  [Invited]

  Nominated symposium


• 2型糖尿病の病態把握におけるMPV(平均血小板容積）の有用性に関する検討

  井上 裕行, 斉藤 真裕美, 胡内 久美子, 吉村 豊, 石田 英和, 中谷 敏也, ASAHARA SHUNICHIROU, KIDO YOSHIAKI, 菊池 英亮

  第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Domestic conference

  Oral presentation


• Progress of inflammation in diabetes patients after total hip and knee arthroplasty

  UESUGI Yuko, HOSONA Mio, KIDO Yoshiaki

  The 20th East Asian Forum of Nursing Scholars, Mar. 2017, English, The Hong Kong Polytechnic University, Hong Kong, China, International conference

  Poster presentation


• 膵β細胞における小胞体ストレスに対するEmodinの効果

  松浦 有希, 松田 友和, 高井 智子, 井上 佳歩, 鈴木 江美, 淺原 俊一郎, 木村 真希, 神野 歩, Kido Yoshiaki

  第39回日本分子生物学会年会, Nov. 2016, Japanese, 日本分子生物学会, 横浜, Domestic conference

  Poster presentation


• 膵α細胞の小胞体ストレス誘導性アポトーシスにおけるCK2βの役割

  高井 智子, 松浦 有希, 井上 佳歩, 神野 歩, 鈴木 江美, 淺原 俊一郎, 松田 友和, Kido Yoshiaki

  第39回日本分子生物学会年会, Nov. 2016, Japanese, 日本分子生物学会, 横浜, Domestic conference

  Poster presentation


• ヒトips細胞を用いた2型糖尿病原因遺伝子による糖尿病発症機序の解明

  下野 名奈子, 淺原 俊一郎, 原 瑞季, 田中 孝一, 松田 友和, 木村 真希, 神野 歩, 高井 智子, 鈴木 江美, Aoi Takashi, Kido Yoshiaki

  第39回日本分子生物学会年会, Nov. 2016, Japanese, 日本分子生物学会, 横浜, Domestic conference

  Poster presentation


• The role of casein kinase 2 in ER stress associated pancreatic β cell failure

  Matsuura Y, Matsuda Takeru, Takai T, Inoue K, Suzuki E, Asahara S, Koyanagi-Kimura M, Kanno A, Kido Yoshiaki

  8th AASD Scientific Meeting, Oct. 2016, English, Taipei, Taiwan, International conference

  Oral presentation


• 膵β細胞不全の分子機構「Regulation of pancreatic beta cell mass through type 2 diabetes susceptibility genes」

  淺原 俊一郎, Kido Yoshiaki

  第59回日本糖尿病学会年次学術集会, May 2016, Japanese, 日本糖尿病学会, 京都, Domestic conference

  [Invited]

  Nominated symposium


• 生物発光イメージング法による生存細胞内小胞体ストレスの定量化

  鈴木 江美, 松田 友和, 川本 剛士, 松浦 有希, 高井 智子, 神野 歩, 木村 真希, 淺原 俊一郎, Ogawa Wataru, Kido Yoshiaki

  第59回日本糖尿病学会年次学術集会, May 2016, Japanese, 日本糖尿病学会, 京都, Domestic conference

  Poster presentation


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  神野 歩, 増田 勝久, 淺原 俊一郎, 松田 友和, 木村 真希, Hirota Yushi, Yokoi Norihide, Ogawa Wataru, Seino Susumu, 春日 雅人, Kido Yoshiaki

  第89回日本内分泌学会学術総会, Apr. 2016, Japanese, 日本内分泌学会, 京都, Domestic conference

  Poster presentation


• 膵β細胞不全関連分子C/EBPβの安定化に対するcasein kinase βの役割

  高井 智子, 松田 友和, 川本 剛士, 松浦 有希, 淺原 俊一郎, 神野 歩, 木村 真希, 鈴木(寺師) 江美, Ogawa Wataru, Kido Yoshiaki

  第38回日本分子生物学会年会, Dec. 2015, Japanese, 日本分子生物学会, 神戸, Domestic conference

  Oral presentation


• C/EBPβの蛋白安定化に関与する新規リン酸化部位の同定

  松浦 有希, 松田 友和, 高井 智子, 川本 剛士, 三枝 祐介, 鈴木(寺師) 江美, 淺原 俊一郎, 木村(小柳) 真希, 神野 歩, Kido Yoshiaki

  第38回日本分子生物学会年会, Dec. 2015, Japanese, 日本分子生物学会, 神戸, Domestic conference

  Poster presentation


• 膵β細胞不全関連因子C/EBPβの発現制御機構の解明

  松浦 有希, 松田 友和, Kido Yoshiaki

  第62回日本臨床検査医学会学術集会, Nov. 2015, Japanese, 日本臨床検査医学会, 岐阜, Domestic conference

  Oral presentation


• Histone deacetylase regulates insulin signaling via two pathways in pancreatic β cells

  Sugiura Y, Asahara S, Kawada Y, Ihara Y, Hara M, Kanno A, Kimura-Koyanagi M, Matsuda T, Seino Susumu, Ogawa Wataru, Kido Yoshiaki

  7th AASD Scientific Meeting and annual Scientific Meeting of the Hong Kong Society of Endocrinology, Metabolism and Reproduction, Nov. 2015, English, Hong Kong, International conference

  Oral presentation


• 2型糖尿病原因遺伝子Kcnq1による膵β細胞量調節機構の解析

  原 瑞季, 淺原 俊一郎, Kido Yoshiaki

  第62回日本臨床検査医学会学術集会, Nov. 2015, Japanese, 日本臨床検査医学会, 岐阜, Domestic conference

  Oral presentation


• GCN2, a type 2 diabetes mellitus susceptibility gene, is associated with the regulation of pancreatic β-cell mass

  Masuda K, Kanno A, Yoshitomi R, Asahara S, Matsuda T, Kimura M, Shibutani Y, Yokoi Norihide, Kasuga M, Seino Susumu, Kido Yoshiaki

  51st EASD Annual Meeting, Sep. 2015, English, Stockholm, Sweden,, International conference

  Oral presentation


• 膵β細胞機能のエピゲノム制御

  Kido Yoshiaki

  関西実験動物研究会第126回研究会, Jun. 2015, Japanese, 関西実験動物研究会, 神戸, Domestic conference

  [Invited]

  Invited oral presentation


• Reduction in Pancreatic β-Cell Mass Caused by Enhanced Expression of Cdkn1c via Interaction between C/EBPβ and Epigenetic Control

  Asahara S, Ihara Y, Inoue H, Teruyama K, Hara M, Kimura M, Matsuda T, Seino Susumu, Kido Yoshiaki

  75th Scientific Session of American Diabetes Association, Jun. 2015, English, Boston, Massachusetts, International conference

  Oral presentation


• GCN2, a Type 2 Diabetes Mellitus Susceptibility Gene, Is Associated with the Regulation of Pancreatic β-Cell Mass

  Kanno A, Masuda K, Asahara S, Kimura M, Matsuda T, Kasuga M, Ogawa Wataru, Seino Susumu, Kido Yoshiaki

  75th Scientific Session of American Diabetes Association, Jun. 2015, English, Boston, Massachusetts, International conference

  Oral presentation


• 膵β細胞不全関連因子CEBPβの発現制御機構の解明

  高井 智子, 松田 友和, 川本 剛士, 松浦 有希, 三枝 祐介, 鈴木 江美, 淺原 俊一郎, 木村 真希, 神野 歩, Kido Yoshiaki

  第58回日本糖尿病学会年次学術集会, May 2015, Japanese, 日本糖尿病学会, 下関, Domestic conference

  Oral presentation


• 膵β細胞における細胞周期調節因子p57の機能解析

  原 瑞季, 淺原 俊一郎, 伊原 佑香, 井上 裕行, 照山 杏子, 松田 友和, 木村 真希, 中山 敬一, Kido Yoshiaki

  第58回日本糖尿病学会年次学術集会, May 2015, Japanese, 日本糖尿病学会, 下関, Domestic conference

  Oral presentation


• 膵β細胞におけるp38経路の活性化は膵島の慢性炎症を惹起することにより膵β細胞不全の病態形成に関与する

  森田 愛梨, Hosooka Tetsuya, 竹村 佑己, 木村 真希, 鈴木 夏実, 淺原 俊一郎, 神野 歩, 松田 友和, Seino Susumu, Kido Yoshiaki

  第58回日本糖尿病学会年次学術集会, May 2015, Japanese, 日本糖尿病学会, 下関, Domestic conference

  Oral presentation


• ヒストン脱アセチル化酵素(HDACs)による膵β細胞量調節機構の解析

  杉浦 佑実子, 淺原 俊一郎, 川田 有希奈, 佐藤 綾香, 木村 真希, 松田 友和, Kido Yoshiaki

  第58回日本糖尿病学会年次学術集会, May 2015, Japanese, 日本糖尿病学会, 下関, Domestic conference

  Poster presentation


• 2型糖尿病疾患感受性遺伝子による膵β細胞量調節機構

  Kido Yoshiaki

  第58回日本糖尿病学会年次学術集会, May 2015, Japanese, 日本糖尿病学会, 下関, Domestic conference

  [Invited]

  Nominated symposium


• 膵β細胞におけるヒストン脱アセチル化酵素HDACの機能解析

  淺原 俊一郎, 杉浦 佑実子, 川田 有希奈, 伊原 佑香, 原 瑞季, 木村 真希, 松田 友和, Seino Susumu, Ogawa Wataru, Kido Yoshiaki

  第88回日本内分泌学会学術総会, Apr. 2015, Japanese, 日本内分泌学会, 東京, Domestic conference

  Poster presentation


• DPP-4阻害薬MK-626が膵β細胞特異的mTORC1活性亢進モデルマウスに及ぼす影響

  木村 真希, 森田 愛梨, 三上 智子, 神野 歩, 松田 友和, 淺原 俊一郎, Seino Susumu, Ogawa Wataru, Kido Yoshiaki

  第88回日本内分泌学会学術総会, Apr. 2015, Japanese, 日本内分泌学会, 東京, Domestic conference

  Poster presentation


• C/EBPβの蛋白安定化に関与する新規リン酸化部位の同定

  川本 剛士, 松田 友和, 三枝 祐介, 高井 智子, 松浦 有希, 淺原 俊一郎, 木村 真希, 神野 歩, Kido Yoshiaki

  第88回日本内分泌学会学術総会, Apr. 2015, Japanese, 日本内分泌学会, 東京, Domestic conference

  Poster presentation


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  増田 勝久, 神野 歩, 淺原 俊一郎, 吉冨 理紗, 松田 友和, 木村 真希, 渋谷 由紀, Hirota Yushi, Yokoi Norihide, 春日 雅人, Seino Susumu, Kido Yoshiaki

  第88回日本内分泌学会学術総会, Apr. 2015, Japanese, 日本内分泌学会, 東京, Domestic conference

  Oral presentation


• 小胞体ストレス関連分子C/EBPβを介した膵β細胞量調節機構の解明

  松田 友和, 三枝 祐介, 川本 剛士, 松浦 有希, 高井 智子, 淺原 俊一郎, 木村 真希, 神野 歩, Ogawa Wataru, Kido Yoshiaki

  第29回日本糖尿病・肥満動物学会年次学術集会, Feb. 2015, Japanese, 日本糖尿病・肥満動物学会, 京都, Domestic conference

  Oral presentation


• 2型糖尿病原因遺伝子Kcnq1と高脂肪食が膵β細胞量に及ぼす相乗的効果の検討

  淺原 俊一郎, 伊原 佑香, 照山 杏子, 原 瑞季, 木村 真希, 松田 友和, 春日 雅人, Seino Susumu, Ogawa Wataru, Kido Yoshiaki

  第29回日本糖尿病・肥満動物学会年次学術集会, Feb. 2015, Japanese, 日本糖尿病・肥満動物学会, 京都, Domestic conference

  Oral presentation


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  神野 歩, 淺原 俊一郎, 増田 勝久, 吉富 理紗, 松田 友和, 木村 真希, 渋谷 由紀, Hirota Yushi, Yokoi Norihide, 春日 雅人, Seino Susumu, Ogawa Wataru, Kido Yoshiaki

  第29回日本糖尿病・肥満動物学会年次学術集会, Feb. 2015, Japanese, 日本糖尿病・肥満動物学会, 京都, Domestic conference

  Oral presentation


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  神野 歩, 増田 勝久, 吉冨 理紗, 淺原 俊一郎, 松田 友和, 木村 真希, 渋谷 由紀, Hirota Yushi, Yokoi Norihide, 春日 雅人, Seino Susumu, Kido Yoshiaki

  第29回日本糖尿病・肥満動物学会, Feb. 2015, Japanese, 日本糖尿病・肥満動物学会, 京都, Domestic conference

  Oral presentation


• 膵β細胞における細胞周期調節蛋白p57の機能解析

  原 瑞季, 淺原 俊一郎, 伊原 佑香, 井上 裕行, 照山 杏子, 松田 友和, 木村(小柳) 真希, 中山 敬一, Kido Yoshiaki

  第37回日本分子生物学会年会, Nov. 2014, Japanese, 日本分子生物学会, 横浜, Domestic conference

  Poster presentation


• 膵β細胞におけるp38経路の活性化は膵島の慢性炎症を惹起することにより膵β細胞不全の病態形成に関与する

  森田 愛梨, Hosooka Tetsuya, 竹村 侑己, 木村(小柳) 真希, 鈴木 夏実, 淺原 俊一郎, 神野 歩, 松田 友和, Seino Susumu, Kido Yoshiaki

  第37回日本分子生物学会年会, Nov. 2014, Japanese, 日本分子生物学会, 横浜, Domestic conference

  Poster presentation


• ヒストン脱アセチル化酵素(HDACs)による膵β細胞量調節機構の解析

  杉浦 佑実子, 淺原 俊一郎, 川田 有希奈, 佐藤 綾香, 木村(小柳) 真希, 松田 友和, Kido Yoshiaki

  第37回日本分子生物学会年会, Nov. 2014, Japanese, 日本分子生物学会, 横浜, Domestic conference

  Poster presentation


• AMPK活性とC/EBPβ発現量のクロストークによる膵β細胞量制御機構

  川本 剛士, 松田 友和, 三枝 祐介, 松浦 有希, 浅原 俊一郎, 木村(小柳) 真希, 神野 歩, Kido Yoshiaki

  第37回日本分子生物学会年会, Nov. 2014, Japanese, 日本分子生物学会, 横浜, Domestic conference

  Poster presentation


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  増田 勝久, 神野 歩, 吉冨 理紗, 淺原 俊一郎, 松田 友和, 木村(小柳) 真希, 渋谷 由紀, Hirota Yushi, Yokoi Norihide, 春日 雅人, Seino Susumu, Kido Yoshiaki

  第37回日本分子生物学会年会, Nov. 2014, Japanese, 日本分子生物学会, 横浜, Domestic conference

  Poster presentation


• Reduction in pancreatic β-cell mass caused by enhanced expression of Cdkn1c via interaction between C/EBPβ and epigenetic control

  Yuka Ihara, Shun-ichiro Asahara, Hiroyuki Inoue, Kyoko Teruyama, Tomokazu Matsuda, Seino Susumu, Kido Yoshiaki

  50th EASD Annual Meeting, Sep. 2014, English, European Association for the Study of Diabetes, Vienna, Austria, International conference

  Poster presentation


• Cross-interaction between C/EBPβ and AMPK determines the pancreatic β-cell mass

  Yusuke Mieda, Takahashi Hiroaki, Tomokazu Matsuda, Shun-ichiro Asahara, Emi Terashi, Ayumi Kanno, Maki Koyanagi, Seino Susumu, Kido Yoshiaki

  50th EASD Annual Meeting, Sep. 2014, English, European Association for the Study of Diabetes, Vienna, Austria, International conference

  Poster presentation


• 膵β細胞のKcnq1遺伝子領域におけるエピジェネティクス制御機構の解析

  伊原 佑香, 淺原 俊一郎, 照山 杏子, 井上 裕行, 江藤 博昭, 木村 真希, 松田 友和, 春日 雅人, Seino Susumu, Kido Yoshiaki

  第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 日本糖尿病学会, 大阪, Domestic conference

  Oral presentation


• AMPK活性依存的なC/EBPβの発現調節による膵β細胞量制御機構

  三枝 祐介, 松田 友和, 高橋 宏昌, 鈴木 江美, 川本 剛士, 淺原 俊一郎, 木村 真希, 神野 歩, Kido Yoshiaki

  第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 日本糖尿病学会, 大阪, Domestic conference

  Oral presentation


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  増田 勝久, 神野 歩, 吉冨 理紗, 淺原 俊一郎, 松田 友和, 木村 真希, 渋谷 由紀, Hirota Yushi, Yokoi Norihide, 春日 雅人, Seino Susumu, Kido Yoshiaki

  第57回日本糖尿病学会年次学術集会, May 2014, Japanese, 日本糖尿病学会, 大阪, Domestic conference

  Oral presentation


• 膵β細胞のKcnq1遺伝子領域におけるエピジェネティクス制御機構の解析

  淺原 俊一郎, 照山 杏子, 井上 裕行, 伊原 佑香, 江藤 博昭, 川田 有希奈, 松田 友和, 春日 雅人, Seino Susumu, Kido Yoshiaki

  第87回日本内分泌学会学術総会, Apr. 2014, Japanese, 日本内分泌学会, 福岡, Domestic conference

  Oral presentation


• 膵β細胞とepigenetics

  Kido Yoshiaki

  第51回日本臨床分子医学会学術集会, Apr. 2014, Japanese, 日本臨床分子医学会, 東京, Domestic conference

  [Invited]

  Nominated symposium


• リン酸化を介したC/EBPβの発現調節による膵β細胞量の制御

  松田 友和, 三枝 祐介, 高橋 宏昌, 川本 剛, 鈴木 江美, 淺原 俊一郎, 木村 真希, 神野 歩, Kido Yoshiaki

  第87回日本内分泌学会学術総会, Apr. 2014, Japanese, 日本内分泌学会, 福岡, Domestic conference

  Oral presentation


• 2型糖尿病感受性遺伝子GCN2は膵β細胞量の調節に関与する

  神野 歩, 吉冨 理紗, 増田 勝久, 淺原 俊一郎, 松田 友和, 木村 真希, 澁谷 由紀, Hirota Yushi, Yokoi Norihide, 春日 雅人, Seino Susumu, Kido Yoshiaki

  第87回日本内分泌学会学術総会, Apr. 2014, Japanese, 日本内分泌学会, 福岡, Domestic conference

  Oral presentation


• 糖尿病患者における非閉塞性腸管虚血症（Nonocculusive mesenteric ischemia: NOMI）－自験例も含めて－

  Kido Yoshiaki, 原 賢太, Yasuda Hisafumi

  第200回日本内科学会近畿地方会, Jun. 2013, Japanese, 日本内科学会, 神戸, 血管の器質的閉塞を認めず腸管の不可逆的虚血を生ずる場合をNOMI(非閉塞性腸管虚血症）といい、早期診断がしばしば困難であり死亡率が高い。糖尿病を基礎疾患として有する場合が多いが、十分に認知されている合併症とは言いがたい。DKAやHHSに伴う報告が多いが、誘因なく発症する報告もあり、腹痛を訴える患者では本疾患の存在を想起し、適切なタイミングで画像診断を行うことが救命のためには重要である。, Domestic conference

  Oral presentation


• 大腸癌のリンパ節転移におけるELF3発現の検討

  半井 千晶, 大澤 佳代, 松原 長秀, 池内 浩基, 鴨志田 伸吾, 岡村 修, 廣田 誠一, 冨田 尚裕, 木戸 良明

  第69回日本癌学会学術総会, Sep. 2010, Japanese, 大阪, Domestic conference

  Poster presentation


• 2型糖尿病患者のコントロール指標に影響する身体活動

  Tsutou Akimitsu, Tamori Yoshikazu, Noguchi Tetsuya, Kido Yoshiaki, Ohara Takeshi, Ogawa Wataru, Miyawaki Ikuko

  第50回日本糖尿病学会年次学術集会, May 2007, Japanese, 日本糖尿病学会, 仙台, Domestic conference

  Oral presentation


• 2型糖尿病患者におけるBMIおよび歩数別の食事摂取量と食事自己管理行動の特徴、

  Tsutou Akimitsu, Tamori Yoshikazu, Noguchi Tetsuya, Kido Yoshiaki, Ohara Takeshi, Ogawa Wataru, Miyawaki Ikuko

  第50回日本糖尿病学会年次学術集会, May 2007, Japanese, 日本糖尿病学会, 仙台, Domestic conference

  Poster presentation


• 2型糖尿病患者におけるBMIおよび歩数別の食事摂取量と食事自己管理行 動の特徴

  Tsutou Akimitsu, Tamori Yoshikazu, Noguchi Tetsuya, Kido Yoshiaki, Ohara Takeshi, Ogawa Wataru, Miyawaki Ikuko

  第50回日本糖尿病学会年次学術集会, May 2007, Japanese, 日本糖尿病学会, 仙台, Domestic conference

  Oral presentation


• ２型糖尿病患者におけるメタボリックシンドローム合併例と非合併例の生活習慣の差異について

  中渡瀬 友里, 多留 ちえみ, 塩谷 英之, 傳 秋光, 木戸 良明, 大原 毅, 宮脇 郁子

  糖尿病合併症（糖尿病合併症19巻Suppl.1 Page93), Sep. 2005, Japanese, Domestic conference

  Oral presentation

• 膵β細胞由来エクソソームによる臓器連関機序の解明

  木戸 良明, 淺原 俊一郎

  日本学術振興会, 科学研究費助成事業, 基盤研究(C), 神戸大学, 01 Apr. 2024 - 31 Mar. 2027


• Elucidation of the pathogenic mechanism of de-differentiation into pancreatic adenocytes in diabetic pancreatic beta cells.

  木村 真希, 木戸 良明, 堀 裕一

  Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Kobe University, 01 Apr. 2023 - 31 Mar. 2026


• 糖尿病患者における水中運動が腎動脈血流量に及ぼす影響

  小野 くみ子, 木戸 良明, 小野寺 昇

  日本学術振興会, 科学研究費助成事業, 基盤研究(C), 神戸大学, 01 Apr. 2021 - 31 Mar. 2024

  【目的】研究課題１は、運動時腎血流の観点から水中運動の利点を明らかにするために、水位の違いが若年健常成人における安静座位時の腎動脈血流に及ぼす影響を明らかにすることを目的とした。 【方法】対象は、健常若年成人男性22名（年齢23.0±1.2歳：平均値±標準偏差）であった。陸上（L）椅子座位安静をとった後、水槽内に移動し、水中椅子座位安静をとった。水中安静時の水位は、大転子（TM）、剣状突起（XP）、頸切痕（JN）と漸増させた。測定項目は、椅子座位安静中の腎動脈血流動態：時間平均血流速度（Vm）・血管抵抗（RI）、血圧（BP）、心拍数（HR）および心臓副交感神経系活動（LnHF）であった。主要評価項目である腎動脈血流動態は、超音波診断装置（超音波診断装置 F37、日立アロカメディカル株式会社）を用いてコンベックス型プローブ（3.0MHz）を使用し、パルスドプラモードにて右腎動脈の血流波形を、全て同一の検者が測定した。対象者の体位はそれぞれ椅子座位とし、プローブを腹部前面に当て、ドプラ入射角は60度以内で測定した。血流測定時、対象者は10秒程度呼吸を止め、3波形分測定し、その平均値を求めた。 【結果】測定環境は、室温29.3±0.8℃、湿度71.2±8.2%、水温33.0±0.6℃、水深はTM 53.4±2.0cm、XP 81.2±2.9cm、JN 98.6±3.0cmであった。水位を上げるに従って、Vmは有意に増加した。RIは有意に増加した。BPは収縮期および拡張期ともに水位の変化に伴う有意な変化は認められなかった。HRは、有意に減少した。LnHFは有意に増大した。 【結論】水位を剣状突起レベルまで上げることによって、腎動脈血流量を増大させることができるものと考えられた。 研究課題１については対象者数を増やして投稿予定であり、研究課題２については、現在遂行中である。


• 膵β細胞におけるインスリンシグナルが可塑性に及ぼす影響の解明

  木戸 良明, 淺原 俊一郎

  日本学術振興会, 科学研究費助成事業, 基盤研究(C), 神戸大学, 01 Apr. 2021 - 31 Mar. 2024

  代表者が独自に作成した膵β細胞特異的Tsc2ノックアウトマウスは、若齢期において膵β細胞量増大、高インスリン血症、低血糖を呈するが、45週齢前後から徐々に血糖上昇を示すことが明らかとなった。その際の膵β細胞量は若齢期と比べて有意に減少しており、またインスリン染色をしたところ膵島内のインスリン陽性細胞が不均一となっていた。既報では、膵β細胞量減少の一機序として脱分化が近年注目されており、本マウスにおいても脱分化が起こっていることが示唆された。しかしながら、膵α細胞量増大は認められず、またインスリン・グルカゴン・PP・ソマトスタチン陰性クロモグラニンA陽性細胞が認められたことから、内分泌ホルモン陰性細胞が膵島内に存在することが明らかとなった。そこで、アミラーゼ染色を行ったところ、膵島内にアミラーゼ陽性細胞が多数認められた。アミラーゼ発現が膵内分泌細胞の脱分化であることを確認するために、若齢期においてPtf1a発現を免疫染色で確認したところ、Ptf1a、クロモグラニンA共発現細胞の存在が確認された。さらにこれらの結果を確認するために、YFPマウスと交配し、Lineage tracingを行ったところ、YFP陽性Ptf1a陽性細胞がTsc2ノックアウトマウスの膵島内においてのみ確認された。また、遺伝子発現変化を確認すべくRNA-seqをしたところ、Tsc2ノックアウトマウスの10週齢ではPdx1やMafA発現が低下しており、Aldh1a3発現が増加していた。これらの結果より、若齢期から脱分化が始まっている可能性が示唆された。


• 日本人2型糖尿病感受性遺伝子GCN2が膵β細胞機能に及ぼす影響に関する検討

  木村 真希, 木戸 良明, 堀 裕一

  日本学術振興会, 科学研究費助成事業, 基盤研究(C), 神戸大学, 01 Apr. 2020 - 31 Mar. 2023

  2型糖尿病の発症・進展には、膵β細胞の質的異常のみならず、膵β細胞量調節機構の異常の関与が明らかとなっている。ヒト被験者における2型糖尿病に関連するGCN2のSNP多型と代謝パラメータとの関係を評価し、リスク対立遺伝子を有する被験者では75gOGTT試験ならびにインスリンクランプ試験にてインスリン分泌が減少していることを見出した。高脂肪食負荷全身性GCN2ノックアウトマウスが耐糖能異常および膵β細胞量減少をきたすこと、およびβ細胞特異的GCN2ノックアウトマウスは高脂肪食負荷後の耐糖能異常および膵β細胞量減少を認めることを既に確認している。GCN2の機能不全が膵β細胞のインスリン分泌能に影響を与えるメカニズムを解明することが本研究の目的である。 当該年度高脂肪食負荷全身性GCN2ノックアウトマウスの膵島およびGCN2ノックダウンINS-1細胞においてSestrin2の発現が低下していることが明らかとなった。このSestrin2がmTORC1活性をネガティブコントロールしていることが培養細胞において確認済である。我々は、mTORC1活性調節に重要なTSC2/14-3-3結合に干渉しうる分子を同定するため、アミノ酸欠損下で培養したコントロールINS-1細胞とGCN2ノックダウンINS-1細胞においてプロテオーム解析を行った。４つの候補分子の中から、L-asparaginaseが糖負荷によりMIN-6細胞および高脂肪食負荷マウスにおいて発現が上昇することを見出した。ここまでの結果において、高脂肪食負荷において、インスリン需要が増大し、膵β細胞におけるインスリン合成が亢進しアミノ酸濃度が減少することにより、GCN2のリン酸化が惹起され、mTORC1活性の調整がSestrin2やL-asparaginaseを介して行われる新たなメカニズムの存在が示唆された。


• 高脂肪食と2型糖尿病感受性遺伝子の相乗効果に関する検討

  木戸 良明

  科学研究費補助金／基盤研究(B), Apr. 2017 - Mar. 2020, Principal investigator

  Competitive research funding


• Elucidatiaon of the role of KAT2A in the regualtion of energy metabolism

  MATSUMOTO MICHIHIRO, KIDO Yoshiaki, INOUE Hiroshi, SAKAI Mashito, MITSUSHIMA Masaru, NAGANUMA Takao, YANO Hiroyuki, YAGI Takashi, MATSUKAWA Toshiya

  Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (B), National Center for Global Health and Medicine, 01 Apr. 2015 - 31 Mar. 2018

  The role of KAT2A in hepatocytes was investigated in the regulation of fasting metabolism using loss-of-function approaches in vivo and in vitro. In the fasted state, hepatic KAT2A formed a signalling module with transcriptional coregulator CITED2 and PKA promoted transcription of fasting response genes, and thereby adapted to fasting. Mechanistically, KAT2A was phosphorylated by PKA within the module, switched its substrate from transcriptional coactivator PGC-1α to histone H3, and thereby promoted activation of this coactivator and epigenomic changes in the promoter, resulting in activation of such gene transcription. These results suggest that KAT2A is a cAMP-responsible acetyltransferase that is critical to integrate fasting metabolic response in hepatocytes.


• 糖尿病患者の人工関節術後感染予防のための患者参加型地域連携血糖管理システムの開発

  上杉 裕子

  学術研究助成基金助成金／基盤研究(C), Apr. 2015 - Mar. 2018

  Competitive research funding


• 超高齢社会における内部障害を有した要介護者に対するコメディカル専門人材養成プログラム開発

  木戸 良明

  文部科学省高等教育局長, 平成29年度「専修学校による地域産業中核的人材養成事業」, 2017, Principal investigator

  Competitive research funding


• 膵β細胞におけるGCN2活性化機序の解明

  木戸 良明

  学術研究助成基金助成金／基盤研究(C), Apr. 2013 - Mar. 2016, Principal investigator

  Competitive research funding


• 超高齢社会における内部障害を有した要介護者に対するコメディカル専門人材養成プログラム開発

  木戸 良明

  文部科学省, 成長分野等における中核的専門人材養成等の戦略的推進事業, 2016, Principal investigator

  Competitive research funding


• Insulin signaling in organs and its integration in mice

  KASUGA Masato, OGAWA Wataru, KIDO Yoshiaki, TAMORI Yoshikazu, NAKAE Jun, INOUE Hiroshi, MATSUMOTO Michihiro

  Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Creative Scientific Research, 2006 - 2010

  We revealed organ-specific insulin signaling by generating mice lacking a fundamental molecule for insulin signaling in an organ-specific manner. These mice also revealed signals used to communicate between organs. For example, we found insulin action in the brain inhibited hepatic glucose production via the nervous system. Thus, homeostasis in a whole body is regulated ingeniously by signals used to communicate within organs and between organs.


• ストレス下におけるＧＣＮ２による膵β細胞量調節機構の解明

  木戸 良明

  科学研究費補助金／基盤研究(C), 2010, Principal investigator

  Competitive research funding


• Identification and clinical application of susceptibility genes for diabetes mellitus.

  KASUGA Masato, KADOWAKI Takashi, YASUDA Kazuki, OOSAWA Haruhiko, NANJO Kishio, KIDO Yoshiaki, MAKINO Eiichi, MIYAKE Kazuaki

  Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research on Priority Areas, Kobe University, 2005 - 2009

  By a genome-wide association study (GWAS) using 100,000 SNPs, we identified KCNQ1 as a novel susceptibility gene for type 2 diabetes mellitus, and performed functional analysis. This turned out to be one of the most important genetic factors in multiple ethnic groups. We also examined other genetic factors for diabetes and found that risk allele frequencies of the SNPs are variable among populations. Furthermore, we reported that the prediction power of all the susceptibility SNPs combined is not sufficient, indicating the existence of unknown genetic factors. We also reported novel diabetes-related genes by candidate gene and candidate region approaches.


• 臓器形成期における飢餓ストレスの膵β細胞への影響

  木戸 良明

  科学研究費補助金／基盤研究(C), 2007, Principal investigator

  Competitive research funding


• 膵β細胞の増殖およびインスリン分泌におけるＰＤＫ‐１の関与に関する研究

  木戸 良明

  科学研究費補助金／基盤研究(C), 2005, Principal investigator

  Competitive research funding