Research activity information

• Apr. 2026 医学生・研修医・専攻医の日本内科学会ことはじめ 2026東京, 優秀指導教官賞


• Apr. 2025 医学生・研修医・専攻医の日本内科学会ことはじめ 2025大阪, 優秀指導教官賞(プレナリーセッション選出)


• May 2010 アジア糖尿病学会, 第2回アジア糖尿病学会 Travel Grant賞


• Mar. 2003 北海道大学, 北海道大学クラーク賞

• Luseogliflozin restores GIP responsiveness in diabetic male mice with preserved β-cell function.

  Quan Yingyue, Harumi Takahashi, Norihide Yokoi, Wataru Ogawa, Kenji Sugawara

  Impaired glucose-dependent insulinotropic polypeptide (GIP)-induced insulin secretion is a characteristic feature of type 2 diabetes, whereas glucagon-like peptide-1 (GLP-1) responsiveness is relatively preserved. Our previous study proposed that chronic β-cell depolarization alters G protein signaling and contributes to this differential incretin responsiveness, but whether glucose lowering by sodium-glucose cotransporter 2 inhibition restores incretin responsiveness remains unclear. We investigated the effects of chronic luseogliflozin treatment on incretin responsiveness in two diabetic mouse models, KK-Ay mice with preserved residual β-cell function and streptozotocin/high-fat diet-induced diabetic mice with severe β-cell impairment. Luseogliflozin improved glycemic control in both models without marked changes in body weight or plasma insulin levels. In KK-Ay mice, luseogliflozin restored the glucose-lowering effect of GIP during GIP-preload glucose tolerance test. In contrast, this effect was not observed in streptozotocin/high-fat diet-induced diabetic mice, suggesting that preserved residual β-cell function is required for recovery of GIP responsiveness. Ex vivo analyses using isolated islets further showed that chronic luseogliflozin treatment altered incretin-stimulated insulin secretion, including attenuation of enhanced GLP-1 responsiveness under diabetic conditions. These findings suggest that luseogliflozin may partially normalize aberrant β-cell incretin signaling and restore GIP responsiveness when sufficient β-cell function remains.

  Jul. 2026, Physiological reports, 14(13) (13), e71016, English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Gene expression profiles associated with stimulus-responsive insulin secretion in insulinoma.

  Kenji Sugawara, Yuko Okada, Tomokazu Matsuda, Yushi Hirota, Shun-Ichiro Asahara, Kazuhiko Sakaguchi, Wataru Ogawa

  Insulinoma is a functional pancreatic neuroendocrine tumor that usually causes fasting hypoglycemia through inappropriate autonomous insulin secretion. However, some insulinomas show postprandial or stimulus-induced hypoglycemia, suggesting that some tumors retain the ability to respond to physiological stimuli. We examined four patients with confirmed insulinoma who showed different clinical patterns of hypoglycemia and integrated clinical stimulation tests with DNA microarray analysis. Insulin secretory dynamics were assessed using an oral glucose tolerance test, meal tolerance test, and glucagon stimulation test, as clinically indicated. Among the four cases, Case 1 showed no clear fasting hypoglycemia but developed hypoglycemia after meals and oral glucose loading, accompanied by marked insulin secretion. In this case, insulin or C-peptide increased markedly after glucose, meal, and glucagon stimulation. In contrast, the other three cases showed relatively weak insulin secretory responses to stimulation. During the fasting test, Cases 3 and 4 developed hypoglycemia early, whereas Case 2 showed a prolonged time to hypoglycemia. Transcriptomic analysis showed that, by hierarchical clustering, Case 1 was clearly separated from Cases 3 and 4, whereas Case 2 was relatively close to Case 1. Case 1 showed relatively preserved expression of genes involved in glucose sensing, ATP-sensitive potassium channel function, incretin/cAMP signaling, exocytosis, and β-cell differentiation. In contrast, cases with predominant fasting hypoglycemia showed higher expression of hexokinase 1 and stress-response genes. These findings suggest that clinical heterogeneity in insulinoma may reflect differences in β-cell-like stimulus-response mechanisms, glucose sensing, stress responses, and differentiation status.

  Jun. 2026, Endocrine connections, English, International magazine

  Scientific journal


• A case of maturity-onset diabetes of the young with a pathogenic HNF1A variant and a coexisting NEUROD1 variant.

  Tomofumi Takayoshi, Yushi Hirota, Kenji Sugawara, Aki Sugano, Mika Ohta, Takehito Takeuchi, Akane Yamamoto, Wataru Satake, Yutaka Takaoka, Wataru Ogawa

  AIMS/INTRODUCTION: Maturity-onset diabetes of the young (MODY) accounts for at least 1%-5% of diabetes cases and is usually caused by single gene variants. Accurate diagnosis of MODY is important for effective management, especially in young individuals who are lean and lack islet autoantibodies. Only a few MODY cases associated with multiple gene variants have been reported. We here describe a rare case of MODY with a pathogenic HNF1A variant and a coexisting NEUROD1 variant. MATERIALS AND METHODS: We conducted an extensive clinical analysis and explored the complex genetic architecture of the case in order to provide insight into the etiology of MODY. The candidate variants were identified by comprehensive whole-exome and Sanger sequencing, and their functional impact was assessed by analysis of their effects on the surface charge or structural stability of HNF1A and NEUROD1. RESULTS: The proband, a 21-year-old woman with early-onset diabetes, was found to harbor a pathogenic HNF1A p.Arg159Trp variant and a coexisting NEUROD1 p.Arg98Ser variant of uncertain significance. The NEUROD1 variant was also present in her mother and sister, both of whom manifested impaired glucose tolerance, but was absent in her father and brother. Structural analyses suggested that the HNF1A variant alters the surface charge of the protein, whereas the NEUROD1 variant may affect protein structural stability. CONCLUSION: We have identified an unusual case of MODY with a pathogenic HNF1A variant and a coexisting NEUROD1 variant of uncertain significance, and structural analyses suggested that the NEUROD1 variant may affect protein structure.

  Jun. 2026, Journal of diabetes investigation, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• A novel small-molecule secretagogue, MDC134, amplifies glucose-dependent insulin secretion in pancreatic β-cells.

  Naoya Murao, Harumi Takahashi, Norihide Yokoi, Kentaro Okano, Okechi S Oduori, Christopher M Carmean, Wataru Ogawa, Kenji Sugawara

  Insulin secretion from pancreatic β-cells is controlled by multiple mechanisms, including metabolic, electrophysiological, and second-messenger pathways. To identify insulinotropic small molecules, we performed in silico similarity screening using zatebradine, an HCN-channel ligand, as a structural query and functionally evaluated 26 hit compounds. Compound 2 showed the strongest insulinotropic activity and was used to synthesize the novel compound MDC134. MDC134 enhanced insulin secretion in MIN6-K8 cells and isolated mouse islets under stimulatory glucose conditions. MDC134 enhanced insulin secretion in isolated mouse islets and showed a tendency to increase insulin secretion in isolated non-diabetic human islets. Under high-glucose conditions, MDC134 increased intracellular Ca2+ levels, and nifedipine abolished its insulinotropic effect, indicating the involvement of voltage-dependent L-type Ca2+ channel-mediated Ca2+ influx. MDC134 also increased cellular cAMP content, although less potently than GLP-1. MDC134 treatment did not clearly affect glucose tolerance in C57BL/6J or ob/ob mice but significantly suppressed glucose elevation in β-cell-specific Kcnj11 knockout mice. These findings identify MDC134 as a novel glucose-dependent insulinotropic small molecule that enhances β-cell insulin secretion through Ca2+ influx and cAMP-associated amplification, and suggest that it may be useful for therapeutic strategies for diabetes characterized by impaired insulin secretion.

  May 2026, Biochemical and biophysical research communications, 823, 153962 - 153962, English, International magazine

  Scientific journal


• CMR12, a novel insulinotropic compound, enhances second-phase insulin secretion with metabolic changes in pancreatic β-cells.

  Kenji Sugawara, Harumi Takahashi, Norihide Yokoi, Wataru Ogawa

  Insulin secretion from pancreatic β-cells is primarily regulated by glucose stimulation, while cAMP-mediated amplifying pathways also play an important role. In this study, we identified compound 42 (C42) as an insulinotropic hit compound through an in silico similarity search using the cAMP analog Sp-cAMPS as a query. Further structural development by chemical synthesis yielded CMR12, a novel derivative with enhanced insulinotropic activity. This class of compounds enhances insulin secretion in MIN6-K8 cells in a glucose concentration-dependent and compound concentration-dependent manner, and shows a modest suppression of glucose excursion during oral glucose tolerance testing in mice. CMR12 also exhibited strong insulinotropic activity in isolated mouse islets and preferentially enhanced the sustained second phase of glucose-stimulated insulin secretion in perfused mouse pancreas. These compounds did not clearly increase Epac2-related FRET responses, intracellular cAMP, or cytosolic Ca2+ levels. CE-MS-based metabolomic analysis of C42-treated MIN6-K8 cells revealed selective metabolic alterations, including increased levels of 2-oxoglutarate and multiple amino acids, without a detectable increase in ATP levels. These findings suggest that CMR12 enhances glucose-stimulated insulin secretion, particularly second-phase secretion, through a mechanism that is not primarily dependent on canonical cAMP- or Ca2+-mediated pathways. CMR12 may serve as a seed compound for developing new therapeutic strategies targeting impaired insulin secretion.

  May 2026, Biochemical and biophysical research communications, 824, 153961 - 153961, English, International magazine

  Scientific journal


• Hemoglobin Trajectories After Metformin Initiation Compared With Dipeptidyl Peptidase-4 Inhibitors: A Real-World Cohort Study.

  Yasuko Morita, Kazuhiko Sakaguchi, Shun-Ichiro Asahara, Wataru Ogawa, Kenji Sugawara

  Background Metformin is associated with vitamin B12 deficiency, and we recently reported latent iron and copper deficiency among metformin users, suggesting a potential contribution to anemia risk. However, real-world evidence on hemoglobin trajectories after metformin initiation remains limited. We evaluated short- and long-term hemoglobin changes after metformin initiation compared with dipeptidyl peptidase-4 (DPP-4) inhibitors in Japanese patients with type 2 diabetes. Methods This single-center retrospective cohort study used electronic medical record data from Kobe University Hospital from January 2014 to June 2025. Short-term hemoglobin changes were defined as changes from Day 0 to Day 180, and long-term trajectories were evaluated from Day 0 to Day 1,826 (five years). Patients initiating metformin or a DPP-4 inhibitor were selected using predefined eligibility and exclusion criteria and matched by propensity scores. Hemoglobin changes over 180 days and up to five years were analyzed using multiple regression and mixed-effects models. Results The short-term cohort included 72 matched pairs, and the long-term cohort included 182 matched pairs. Hemoglobin decreased from 14.74 ± 0.22 to 14.39 ± 0.23 g/dL (mean ± SEM) from Day 0 to Day 180 in the metformin group, whereas no significant change was observed in the DPP-4 inhibitor group. Pre-initiation hemoglobin change, but not metformin dose, was independently associated with subsequent hemoglobin change. Over five years, annual hemoglobin slopes did not differ significantly between groups (-0.0572 vs. -0.0725 g/dL/year, p = 0.31). Older patients showed more negative annual hemoglobin slopes in both groups. Conclusions Metformin initiation was associated with a short-term hemoglobin decrease, whereas excess long-term decline was not observed in this cohort. Long-term changes were modest and age-related, supporting continued monitoring in older patients.

  May 2026, Cureus, 18(5) (5), e109639, English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• The role of CXCL10 in high-fat diet-induced skeletal muscle inflammation and atrophy.

  An Liyuan, Yu Hirata, Tomoya Inoue, Kenji Sugawara, Wataru Ogawa

  AIMS/INTRODUCTION: Obesity is often accompanied by skeletal muscle atrophy, which aggravates insulin resistance and metabolic dysfunction. Chronic inflammation is implicated in this process, but the molecular mediators linking obesity-induced inflammation to muscle wasting have remained unclear. We investigated the role of the chemokine CXCL10 in skeletal muscle inflammation and atrophy induced by a high-fat diet (HFD). MATERIALS AND METHODS: Male C57BL/6J mice were fed an HFD or normal diet for 2 weeks and received either neutralizing antibodies to CXCL10 or control immunoglobulin G. Muscle morphology, macrophage infiltration, and gene expression were examined by histology, immunohistochemistry, reverse transcription-quantitative polymerase chain reaction analysis, and RNA sequencing. Cultured C2C12 myotubes were also treated with recombinant CXCL10 or lipopolysaccharide (LPS), with or without antibodies to CXCL10, for assessment of direct effects on myotube atrophy. RESULTS: HFD feeding upregulated Cxcl10 expression in skeletal muscle. It also induced fiber atrophy, macrophage infiltration, and increased expression of individual inflammation- or proteolysis-related genes in muscle, with these effects being attenuated by CXCL10 neutralization. Transcriptomic analysis further revealed a broad reversal of HFD-induced changes in gene expression related to protein catabolism and myofiber structure by anti-CXCL10 administration. Both CXCL10 and LPS reduced myotube diameter and increased expression of catabolism- or inflammation-related genes in cultured C2C12 myotubes, whereas CXCL10 blockade prevented these effects of LPS. CONCLUSIONS: CXCL10 mediates HFD-induced skeletal muscle atrophy by promoting inflammation and proteolysis. CXCL10 neutralization mitigates such muscle loss and may represent a novel therapeutic strategy to preserve skeletal muscle mass under metabolic stress.

  Feb. 2026, Journal of diabetes investigation, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Similarities and Differences in the Intestinal Actions of Metformin and Imeglimin

  Kenji Sugawara, Kaori Hozumi, Hiroshi Mizuma, Daisuke Sasaki, Masakazu Shinohara, Akihiko Kondo, Yasuyoshi Watanabe, Wataru Ogawa

  Lead, Sep. 2025, Diabetes, Obesity and Metabolism

  [Refereed]

  Link to Kobe Univ. Repository (Kernel)


• Association of metformin treatment with changes in metal dynamics in individuals with type 2 diabetes.

  Natsu Otowa-Suematsu, Kazuhiko Sakaguchi, Tomoko Yamada, Marika Nishisaka, Yasuko Morita, Hayato Fukumitsu, Yukari Katsura, Yuko Okada, Yushi Hirota, Kenji Sugawara, Wataru Ogawa

  INTRODUCTION: The metal-chelating activity of metformin, which has long been known but of unclear clinical relevance, has recently been implicated in the pleiotropic effects, including antitumorigenic and anti-inflammatory actions, of the drug. However, whether metformin actually influences metal dynamics in humans has remained unknown. We here investigate whether metformin influences serum metal levels in individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS: In this cross-sectional study, individuals with type 2 diabetes treated or not treated with metformin for at least 6 months were recruited. The primary outcome was the difference in serum copper concentration between metformin users and non-users. Secondary outcomes included differences in serum levels of iron, zinc, and vitamin B12 as well as in copper-related and iron-related parameters between the two groups. RESULTS: A total of 189 individuals (93 metformin users and 96 non-users) were analyzed. Metformin users showed significantly lower serum copper (16.0 vs 17.8 µmol/L, p<0.001) and iron levels (16.3 vs 17.3 µmol/L, p=0.02) and higher zinc levels (13.3 vs 12.5 µmol/L, p=0.01) compared with non-users. Copper-related and iron-related parameters for metformin users were consistent with latent deficiencies of these metals. Serum homocysteine levels (12.2 vs 11.2 µmol/L, p=0.03) were significantly higher, whereas vitamin B12 levels (338.7 vs 412.8 pmol/L, p<0.001) were significantly lower, in metformin users. Multiple regression analysis including variables that potentially influence metal dynamics identified metformin use as an independent predictor of serum copper (B = -1.54 µmol/L, p<0.001) and iron levels (B = -2.49 µmol/L, p=0.004). CONCLUSIONS: Metformin use was associated with reduced serum levels of copper and iron, as well as with increased serum zinc levels. These changes in metal dynamics may be related to the pharmacological effects of this widely administered drug.

  Aug. 2025, BMJ open diabetes research & care, 13(5) (5), English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Glucocorticoid Resistance Syndrome as a Hidden Cause of Nonneoplastic Hypercortisolism.

  Naoki Yamamoto, Nozomi Kido, Kenji Sugawara, Hironori Bando, Masaaki Yamamoto, Shin Urai, Yasutaka Tsujimoto, Yuka Ohmachi, Yuma Motomura, Yuka Oi-Yo, Yuriko Sasaki, Masaki Suzuki, Michiko Takahashi, Genzo Iguchi, Wataru Ogawa, Hidenori Fukuoka

  Cases of hypercortisolemia without physical signs of Cushing's syndrome (CS), suggestive of nonneoplastic hypercortisolism (NNH), often remain partially unexplained. We present a unique case that was initially misdiagnosed as ACTH-dependent CS due to abnormal laboratory findings, despite the absence of Cushingoid features. Molecular and functional analyses ultimately led to a diagnosis of glucocorticoid resistance syndrome (GRS). A 54-year-old female patient underwent endocrinological evaluation for an adrenal incidentaloma associated with hypokalemia, which revealed hypercortisolemia. Subsequent endocrinological testing was consistent with ACTH-dependent CS; however, no Cushingoid features were observed on physical examination, suggesting NNH. As no apparent cause of NNH was identified, we hypothesized a functional disorder of the glucocorticoid receptor (GR) and performed a genetic analysis of NR3C1, which encodes GR. This revealed a novel germline heterozygous variant, p.L670P, located in the ligand-binding domain of the GR. Structural analyses revealed that Leu670 forms a hydrophobic core near the ligand-binding pocket. The p.L670P variant disrupted the secondary structure, suggesting a potential compromise in the structural stability of the ligand-binding site. In vitro experiments showed that this GR variant failed to suppress the transcriptional activity of the proopiomelanocortin promoter following dexamethasone administration. These findings confirmed that the patient had a loss-of-function variant in GR, leading to a diagnosis of GRS and ruling out ACTH-dependent CS. This case highlights that GRS may underline cases of NNH without a clear etiology, and genetic testing for GR can aid in its diagnosis.

  Jul. 2025, Journal of the Endocrine Society, 9(7) (7), bvaf097, English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• PIK3R1 mutations in individuals with insulin resistance or growth retardation: Case series and in silico functional analysis.

  Tomofumi Takayoshi, Yushi Hirota, Aki Sugano, Kenji Sugawara, Takehito Takeuchi, Mika Ohta, Kai Yoshimura, Seiji Nishikage, Akane Yamamoto, Yu Mimura, Shinji Higuchi, Jun Mori, Rie Kawakita, Tohru Yorifuji, Yutaka Takaoka, Wataru Ogawa

  AIMS/INTRODUCTION: Phosphatidylinositol 3-kinase (PI3K) plays a key role in insulin signaling, and mutations in PIK3R1, which encodes a regulatory subunit (p85α) of this enzyme, are responsible for SHORT syndrome, which is associated with insulin-resistant diabetes. We here describe four Japanese individuals from three families with SHORT syndrome who harbor either a common or a previously unknown mutation in PIK3R1 as well as provide an in silico functional analysis of the mutant proteins. MATERIALS AND METHODS: Gene sequencing was performed to identify PIK3R1 mutations. 3D structural analysis of wild-type and mutant p85α proteins was performed by homology modeling, and structural optimization and molecular dynamics simulations confirmed stable trajectories. Docking simulations of p85α with a phosphopeptide were also conducted. RESULTS: We identified two families with a common mutation (c.1945C>T, p.R649W) and one family with a previously unidentified mutation (c.1957A>T, p.K653*) of PIK3R1. In silico modeling revealed that both mutations impaired binding of p85α to phosphopeptide, with K653* resulting in the loss of amino acids that contribute to such binding. Docking simulations showed a significant loss of docking energy for the R649W mutant compared with the wild-type protein (P = 0.00329). CONCLUSIONS: The four cases of SHORT syndrome were associated with early-onset diabetes and intrauterine growth retardation, with the identified mutations likely disrupting the binding of p85α to phosphopeptide and thereby impairing insulin signaling. One case uniquely manifested diabetes without insulin resistance, emphasizing the need for further study of the clinical variability of SHORT syndrome, especially with regard to its associated diabetes.

  May 2025, Journal of diabetes investigation, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Effects of Systemic and Skeletal Muscle-Specific Overexpression of Piezo1.

  Tomoya Inoue, Tomoko Nishigaki, Yu Hirata, Kazuhiro Nomura, Kenji Sugawara, Wataru Ogawa

  Piezo1, a mechanosensitive ion channel that opens in response to mechanical stimuli, is widely expressed among mammalian cell types, and regulates a diverse range of physiological processes. Although evidence has suggested potential clinical benefit of Piezo1 activation for various conditions, the safety and efficacy of such activation in living animals have remained unclear. To investigate the therapeutic potential of Piezo1 activation, we here generated genetically modified mouse models in which Piezo1 is overexpressed either specifically in skeletal muscle or systemically in response to tamoxifen treatment in adult animals. Cast immobilization induced a reduction in both muscle mass and the abundance of Piezo1 mRNA in skeletal muscle of the affected limbs in control mice. Overexpression of Piezo1 in skeletal muscle prevented the immobilization-induced reduction both in soleus muscle mass and in the corresponding cross-sectional area of myofibers, suggesting the potential benefit of Piezo1 activation for prevention of immobilization-induced muscle atrophy. Furthermore, mice with systemic overexpression of Piezo1 showed no apparent abnormalities in growth or general activity. Red blood cells from these mice manifested slight resistance to hypoosmolarity-induced hemolysis, and the animals did not develop apparent hemolytic anemia. Our findings demonstrate promising efficacy and safety of Piezo1 activation in living animals and thereby highlight the therapeutic potential of targeting the Piezo1 signaling pathway.

  May 2025, The Kobe journal of medical sciences, 71(1) (1), E31-E40, English, Domestic magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Metformin-regulated glucose flux from the circulation to the intestinal lumen.

  Kazuhiko Sakaguchi, Kenji Sugawara, Yusei Hosokawa, Jun Ito, Yasuko Morita, Hiroshi Mizuma, Yasuyoshi Watanabe, Yuichi Kimura, Shunsuke Aburaya, Masatomo Takahashi, Yoshihiro Izumi, Takeshi Bamba, Hisako Komada, Tomoko Yamada, Yushi Hirota, Masaru Yoshida, Munenobu Nogami, Takamichi Murakami, Wataru Ogawa

  BACKGROUND: Through a retrospective analysis of existing FDG PET-MRI images, we recently demonstrated that metformin increases the accumulation of FDG in the intestinal lumen, suggesting that metformin stimulates glucose excretion into the intestine. However, the details of this phenomenon remain unclear. We here investigate the detailed dynamics of intestinal glucose excretion, including the rate of excretion and the metabolism of excreted glucose, in both the presence and absence of metformin. METHODS: We quantified intestinal glucose excretion using newly developed FDG PET-MRI-based bioimaging in individuals with type 2 diabetes, both treated and untreated with metformin. The metabolism of excreted glucose was analyzed through mass spectrometry of fecal samples from mice intravenously injected with 13C-labeled glucose. RESULTS: Continuous FDG PET/MRI image taking reveals that FDG is initially observed in the jejunum, suggesting its involvement in FDG excretion. Metformin-treated individuals excrete a significant amount of glucose (~1.65 g h-1 per body) into the intestinal lumen. In individuals not receiving metformin, a certain amount of glucose (~0.41 g h-1per body) is also excreted into the intestinal lumen, indicating its physiological importance. Intravenous injection of 13C-labeled glucose in mice increases the content of 13C in short-chain fatty acids (SCFAs) extracted from feces, and metformin increased the incorporation of 13C into SCFAs. CONCLUSIONS: A previously unrecognized, substantial flux of glucose from the circulation to the intestinal lumen exists, which likely contributes to the symbiosis between gut microbiota and the host. This flux represents a potential target of metformin's action in humans.

  Mar. 2025, Communications medicine, 5(1) (1), 44 - 44, English, International magazine

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Efficacy of asfotase alfa in a patient with adult-onset hypophosphatasia without obvious bone lesions: a case report with review of literature

  Seiji Nishikage, Masaaki Yamamoto, Takahiro Niikura, Yuiko Inaba, Tomoyuki Akiyama, Risa Harada, Yoshitada Sakai, Kenji Sugawara, Kanako Tachikawa, Toshimi Michigami, Wataru Ogawa, Hidenori Fukuoka

  Japan Endocrine Society, 2025, Endocrine Journal

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Stimulatory effect of imeglimin on incretin secretion.

  Quan Yingyue, Kenji Sugawara, Harumi Takahashi, Norihide Yokoi, Kento Ohbayashi, Yusaku Iwasaki, Susumu Seino, Wataru Ogawa

  AIMS/INTRODUCTION: Imeglimin is a new antidiabetic drug structurally related to metformin. Despite this structural similarity, only imeglimin augments glucose-stimulated insulin secretion (GSIS), with the mechanism underlying this effect remaining unclear. Given that glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) also enhance GSIS, we examined whether these incretin hormones might contribute to the pharmacological actions of imeglimin. MATERIALS AND METHODS: Blood glucose and plasma insulin, GIP, and GLP-1 concentrations were measured during an oral glucose tolerance test (OGTT) performed in C57BL/6JJcl (C57BL/6) or KK-Ay/TaJcl (KK-Ay) mice after administration of a single dose of imeglimin with or without the dipeptidyl peptidase-4 inhibitor sitagliptin or the GLP-1 receptor antagonist exendin-9. The effects of imeglimin, with or without GIP or GLP-1, on GSIS were examined in C57BL/6 mouse islets. RESULTS: Imeglimin lowered blood glucose and increased plasma insulin levels during an OGTT in both C57BL/6 and KK-Ay mice, whereas it also increased the plasma levels of GIP and GLP-1 in KK-Ay mice and the GLP-1 levels in C57BL/6 mice. The combination of imeglimin and sitagliptin increased plasma insulin and GLP-1 levels during the OGTT in KK-Ay mice to a markedly greater extent than did either drug alone. Imeglimin enhanced GSIS in an additive manner with GLP-1, but not with GIP, in mouse islets. Exendin-9 had only a minor inhibitory effect on the glucose-lowering action of imeglimin during the OGTT in KK-Ay mice. CONCLUSIONS: Our data suggest that the imeglimin-induced increase in plasma GLP-1 levels likely contributes at least in part to its stimulatory effect on insulin secretion.

  Jun. 2023, Journal of diabetes investigation, 14(6) (6), 746 - 755, English, Domestic magazine

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• A novel view of the insulin signaling pathway based on prediction of protein structure by the AI platform AlphaFold.

  Kyosuke Sato, Kenji Sugawara, Wataru Ogawa

  The predicted structures of major proteins involved in the insulin signaling pathway obtained from the AlphaFold Protein Structure Database.

  Corresponding, Feb. 2023, Journal of diabetes investigation, English, Domestic magazine

  [Refereed][Invited]

  Link to Kobe Univ. Repository (Kernel)


• Effects of imeglimin on mitochondrial function, AMPK activity, and gene expression in hepatocytes.

  Kaori Hozumi, Kenji Sugawara, Takaya Ishihara, Naotada Ishihara, Wataru Ogawa

  Imeglimin is a recently launched antidiabetic drug structurally related to metformin. To provide insight into the pharmacological properties of imeglimin, we investigated its effects on hepatocytes and compared them with those of metformin. The effects of imeglimin on mitochondrial function in HepG2 cells or mouse primary hepatocytes were examined with an extracellular flux analyzer and on gene expression in HepG2 cells by comprehensive RNA-sequencing analysis. The effects of the drug on AMPK activity in HepG2 cells, mouse primary hepatocytes, and mouse liver were also examined. Treatment of HepG2 cells or mouse primary hepatocytes with imeglimin reduced the oxygen consumption rate coupled to ATP production. Imeglimin activated AMPK in these cells whereas the potency was smaller than metformin. Bolus administration of imeglimin in mice also activated AMPK in the liver. Whereas the effects of imeglimin and metformin on gene expression in HepG2 cells were similar overall, the expression of genes encoding proteins of mitochondrial respiratory complex III and complex I was upregulated by imeglimin but not by metformin. Our results suggest that imeglimin and metformin exert similar pharmacological effects on mitochondrial respiration, AMPK activity, and gene expression in cultured hepatocytes, whereas the two drugs differ in their effects on the expression of certain genes related to mitochondrial function.

  Jan. 2023, Scientific reports, 13(1) (1), 746 - 746, English, International magazine

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• New mechanism of metformin action mediated by lysosomal presenilin enhancer 2.

  Kenji Sugawara, Wataru Ogawa

  Formation of the PEN2-ATP6AP1 complex induced by the binding of metformin to PEN2 results in the inhibition of v-ATPase activity and in the recruitment of AXIN/LKB1 to lysosomes, which in turn results in the phosphorylation and activation of AMPK.

  Lead, Oct. 2022, Journal of diabetes investigation, English, Domestic magazine

  [Refereed][Invited]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• A case of α-chain variant hemoglobin (Hb Chad) with falsely high HbA1c levels measured by immunoassay.

  Kei Yoshino, Yushi Hirota, Wataru Ogawa, Kenji Sugawara, Akira Kawaguchi, Hiroshi Yoshino, Midori Ishibashi, Gen Yoshino, Masafumi Koga

  Variant hemoglobin is often detected during the diagnosis and treatment of diabetes mellitus. We here describe a case of α2-chain variant hemoglobin (Hb Chad) that was identified as a result of differences in HbA1cs values determined by different assays. HbA1c measured by immunoassay was thus falsely high, whereas that measured by high-performance liquid chromatography (HPLC) was slightly low. Sequencing analysis revealed a heterozygous GAG (glutamic acid) → AAG (lysine) mutation at amino acid position 23 of the α2-globin gene. This residue is located at the surface of the α-chain in the crystal structure of hemoglobin. The high HbA1c value determined by immunoassay might have been the result of increased antigenicity of the variant hemoglobin, whereas the low value measured by HPLC reflected differential fractionation of the variant relative to the wild-type protein. Hb Chad has been reported in only three cases to date, and HbA1c was measured for the first time. This is the first case where falsely high HbA1c measured by immunoassay due to increased antigenicity in α-chain variant hemoglobin. This case highlights the importance of comparison with other parameters related to plasma glucose such as glycated albumin if an HbA1c abnormality is suspected. Supplementary Information: The online version contains supplementary material available at 10.1007/s13340-021-00529-y.

  Springer Science and Business Media LLC, Jan. 2022, Diabetology international, 13(1) (1), 330 - 335, English, Domestic magazine

  [Refereed]

  Scientific journal


• The gut microbial metabolite imidazole propionate inhibits metformin action.

  Kenji Sugawara, Wataru Ogawa

  Imidazole propionate inhibits metformin action in a manner dependent on a p38γ-Akt-AMPK axis.

  Corresponding, May 2021, Journal of diabetes investigation, 12(8) (8), 1319 - 1321, English, Domestic magazine

  [Refereed][Invited]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• Dose-dependent accumulation of glucose in the intestinal wall and lumen induced by metformin as revealed by 18 F-labelled fluorodeoxyglucose positron emission tomography-MRI.

  Jun Ito, Munenobu Nogami, Yasuko Morita, Kazuhiko Sakaguchi, Hisako Komada, Yushi Hirota, Kenji Sugawara, Yoshikazu Tamori, Feibi Zeng, Takamichi Murakami, Wataru Ogawa

  AIM: To investigate the relationships between various clinical variables and the metformin-induced accumulation of fluorodeoxyglucose (FDG) in the intestine, with distinction between the intestinal wall and lumen, in individuals with type 2 diabetes who were receiving metformin treatment and underwent 18 F-labelled FDG ([18 F]FDG) positron emission tomography (PET)-MRI. MATERIALS AND METHODS: We evaluated intestinal accumulation of [18 F]FDG with both subjective (a five-point visual scale determined by two experienced radiologists) and objective analyses (measurement of the maximum standardized uptake value [SUVmax ]) in 26 individuals with type 2 diabetes who were receiving metformin and underwent [18 F]FDG PET-MRI. [18 F]FDG accumulation within the intestinal wall was discriminated from that in the lumen on the basis of SUVmax . RESULTS: SUVmax for the large intestine was correlated with blood glucose level (BG) and metformin dose, but not with age, body mass index, HbA1c level or estimated glomerular filtration rate (eGFR). SUVmax for the small intestine was not correlated with any of these variables. Visual scale analysis yielded essentially similar results. Metformin dose and eGFR were correlated with SUVmax for the wall and lumen of the large intestine, whereas BG was correlated with that for the wall. Multivariable analysis identified metformin dose as an explanatory factor for SUVmax in the wall and lumen of the large intestine after adjustment for potential confounders including BG and eGFR. CONCLUSIONS: Metformin dose is an independent determinant of [18 F]FDG accumulation in the wall and lumen of the large intestine in individuals treated with this drug.

  Mar. 2021, Diabetes, obesity & metabolism, 23(3) (3), 692 - 699, English, International magazine

  [Refereed]

  Scientific journal


• Enhanced Release of Glucose Into the Intraluminal Space of the Intestine Associated With Metformin Treatment as Revealed by [18F]Fluorodeoxyglucose PET-MRI.

  Morita Y, Nogami M, Sakaguchi K, Okada Y, Hirota Y, Sugawara K, Tamori Y, Zeng F, Murakami T, Ogawa W

  OBJECTIVE: Positron emission tomography (PET)-computed tomography has revealed that metformin promotes the intestinal accumulation of [18F]fluorodeoxyglucose (FDG), a nonmetabolizable glucose derivative. It has remained unknown, however, whether this accumulation occurs in the wall or intraluminal space of the intestine. We here addressed this question with the use of [18F]FDG PET-MRI, a recently developed imaging method with increased accuracy of registration and high soft-tissue contrast. RESEARCH DESIGN AND METHODS: Among 244 individuals with type 2 diabetes who underwent PET-MRI, we extracted 24 pairs of subjects matched for age, BMI, and HbA1c level who were receiving treatment with metformin (metformin group) or were not (control group). We evaluated accumulation of [18F]FDG in different portions of the intestine with both a visual scale and measurement of maximum standardized uptake value (SUVmax), and such accumulation within the intestinal wall or lumen was discriminated on the basis of SUVmax. RESULTS: SUVmax of the jejunum, ileum, and right or left hemicolon was greater in the metformin group than in the control group. [18F]FDG accumulation in the ileum and right or left hemicolon, as assessed with the visual scale, was also greater in the metformin group. SUVmax for the intraluminal space of the ileum and right or left hemicolon, but not that for the intestinal wall, was greater in the metformin group than in the control group. CONCLUSIONS: Metformin treatment was associated with increased accumulation of [18F]FDG in the intraluminal space of the intestine, suggesting that this drug promotes the transport of glucose from the circulation into stool.

  Jul. 2020, Diabetes Care, 43(7) (7), 1 - 7, English, International magazine

  [Refereed]

  Scientific journal


• Relation between metformin use and vitamin B12 status in patients with type 2 diabetes in Japan

  Sugawara K, Okada Y, Hirota Y, Sakaguchi K, Ogawa W

  Lead, Dec. 2019, Journal of Diabetes Investigation

  [Refereed]


• Phenotypic differences and similarities of monozygotic twins with maturity-onset diabetes of the young type 5.

  Yasuko Ohara, Yuko Okada, Tomoko Yamada, Kenji Sugawara, Masayuki Kanatani, Hidenori Fukuoka, Yushi Hirota, Takaki Maeda, Naoya Morisada, Kazumoto Iijima, Wataru Ogawa

  Here, we report phenotypic differences and similarities of monozygotic twins with maturity-onset diabetes of the young type 5 harboring a partial deletion of chromosome 17q12. The proband and her twin sister manifested complete aplasia and marked hypoplasia, respectively, of the body and tail of the pancreas. Whereas both twins showed marked hypoplasia of the right kidney and multiple cysts in both kidneys, only the proband's sister showed hydronephrosis in the left kidney. The proband had profound defects in insulin and glucagon secretion, as well as mild renal dysfunction, whereas her sister had pronounced renal dysfunction accompanied by mild defects in insulin and glucagon secretion. Both twins manifested hypomagnesemia and hyperuricemia, but no apparent liver dysfunction or intellectual disability. The severity of renal and pancreatic defects differed between monozygotic twins with maturity-onset diabetes of the young type 5, suggesting that the phenotypes of this condition are determined not solely by genetic factors.

  Jul. 2019, Journal of diabetes investigation, 10(4) (4), 1112 - 1115, English, Domestic magazine

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• In silico and in vitro analyses of the pathological relevance of the R258H mutation of hepatocyte nuclear factor 4α identified in MODY1.

  Sugawara K, Nomura K, Okada Y, Sugano A, Matsumoto M, Takarada T, Takeuchi A, Awano H, Hirota Y, Nishio H, Takaoka Y, Ogawa W

  Mutations of the hepatocyte nuclear factor 4α (HNF4α) gene give rise to maturity-onset diabetes of the young type 1. Although many such mutations have been identified in affected individuals, part of these mutations has been characterized with regard to their pathological relevance. We here identified a missense mutation (c.773G>A, p.R258H) of HNF4A in a mother and daughter with early-onset diabetes and impaired insulin secretion. In silico simulation and in vitro luciferase reporter analyses showed that the mutation impairs the stability of self-dimerization and the transactivation activity of HNF4α. Although arginine-258 does not appear to participate directly in dimerization, its mutation alters the electrostatic surface potential of the dimer interface. Our results thus suggest that this mutation impairs the function of HNF4α and thereby contributes to the pathogenesis of maturity-onset diabetes of the young type 1.

  Lead, Oct. 2018, Journal of Diabetes Investigation, 10(3) (3), 680 - 684, English, Domestic magazine

  [Refereed]

  Scientific journal

  Link to Kobe Univ. Repository (Kernel)


• beta-Cell signalling and insulin secretagogues: A path for improved diabetes therapy

  Susumu Seino, Kenji Sugawara, Norihide Yokoi, Harumi Takahashi

  Sep. 2017, DIABETES OBESITY & METABOLISM, 19, 22 - 29, English

  [Refereed]


• A Novel Diphenylthiosemicarbazide Is a Potential Insulin Secretagogue for Anti-Diabetic Agent

  Kenji Sugawara, Kohei Honda, Yoshie Reien, Norihide Yokoi, Chihiro Seki, Harumi Takahashi, Kohtaro Minami, Ichiro Mori, Akio Matsumoto, Haruaki Nakaya, Susumu Seino

  Lead, Oct. 2016, PLOS ONE, 11(10) (10), e0164785, English

  [Refereed]

  Scientific journal


• Structure and functional roles of Epac2 (Rapgef4)

  Kenji Sugawara, Tadao Shibasaki, Harumi Takahashi, Susumu Seino

  Lead, Jan. 2016, GENE, 575(2) (2), 577 - 583, English

  [Refereed]


• Glutamate Acts as a Key Signal Linking Glucose Metabolism to Incretin/cAMP Action to Amplify Insulin Secretion

  Ghupurjan Gheni, Masahito Ogura, Masahiro Iwasaki, Norihide Yokoi, Kohtaro Minami, Yasumune Nakayama, Kazuo Harada, Benoit Hastoy, Xichen Wu, Harumi Takahashi, Kazushi Kimura, Toshiya Matsubara, Ritsuko Hoshikawa, Naoya Hatano, Kenji Sugawara, Tadao Shibasaki, Nobuya Inagaki, Takeshi Bamba, Akira Mizoguchi, Eiichiro Fukusaki, Patrik Rorsman, Susumu Seino

  Oct. 2014, CELL REPORTS, 9(2) (2), 661 - 673, English

  [Refereed]

  Scientific journal


• Antidiabetic Sulfonylureas and cAMP Cooperatively Activate Epac2A

  Toshimasa Takahashi, Tadao Shibasaki, Harumi Takahashi, Kenji Sugawara, Aika Ono, Naoko Inoue, Toshio Furuya, Susumu Seino

  Oct. 2013, SCIENCE SIGNALING, 6(298) (298), ra94, English

  [Refereed]

  Scientific journal


• Predicting efficacy of dipeptidyl peptidase-4 inhibitors in patients with type 2 diabetes: Association of glycated hemoglobin reduction with serum eicosapentaenoic acid and docosahexaenoic acid levels

  Masahiro Iwasaki, Fuminori Hoshian, Tomoko Tsuji, Naoki Hirose, Tomoko Matsumoto, Naomi Kitatani, Kenji Sugawara, Ryota Usui, Hitoshi Kuwata, Kazu Sugizaki, Yuka Kitamoto, Shuichi Fujiwara, Koin Watanabe, Takanori Hyo, Takeshi Kurose, Yutaka Seino, Daisuke Yabe

  Oct. 2012, JOURNAL OF DIABETES INVESTIGATION, 3(5) (5), 464 - 467, English

  [Refereed]

  Scientific journal


• Comparison of incretin immunoassays with or without plasma extraction: Incretin secretion in Japanese patients with type 2 diabetes

  Daisuke Yabe, Koin Watanabe, Kenji Sugawara, Hitoshi Kuwata, Yuka Kitamoto, Kazu Sugizaki, Shuichi Fujiwara, Masahiro Hishizawa, Takanori Hyo, Kyoko Kuwabara, Kayo Yokota, Masahiro Iwasaki, Naomi Kitatani, Takeshi Kurose, Nobuya Inagaki, Yutaka Seino

  Feb. 2012, JOURNAL OF DIABETES INVESTIGATION, 3(1) (1), 70 - 79, English

  [Refereed]

  Scientific journal


• A case of triple cancer of the pancreas, colon, and peripheral nerve sheath in type 2 diabetes found by progressive body weight loss and deteriorating glycemic control

  Rokutan M, Yabe D, Usui R, Sugawara K, Kitamoto Y, Kuwata H, Sugizaki K, Fujiwara S, Watanabe K, Hyo T, Kawai J, Hosoda Y, Awane M, Taki Y, Tachi H, Ueda Y, Mizuno H, Kurose T, Seino Y

  THE JAPAN DIABETES SOCIETY, 2012, Journal of the Japan Diabetes Society, 55(7) (7), 477 - 482, Japanese

  [Refereed]


• Rab11 and its effector Rip11 participate in regulation of insulin granule exocytosis

  Kenji Sugawara, Tadao Shibasaki, Akira Mizoguchi, Tetsuya Saito, Susumu Seino

  Lead, Apr. 2009, GENES TO CELLS, 14(4) (4), 445 - 456, English

  [Refereed]

  Scientific journal


• Structural basis for the specificity and catalysis of human Atg4B responsible for mammalian autophagy

  K Sugawara, NN Suzuki, Y Fujioka, N Mizushima, Y Ohsumi, F Inagaki

  Lead, Dec. 2005, JOURNAL OF BIOLOGICAL CHEMISTRY, 280(48) (48), 40058 - 40065, English

  [Refereed]

  Scientific journal


• The crystal structure of microtubule-associated protein light chain 3, a mammalian homologue of Saccharomyces cerevisiae Atg8

  K Sugawara, NN Suzuki, Y Fujioka, N Mizushima, Y Ohsumi, F Inagaki

  Lead, Jul. 2004, GENES TO CELLS, 9(7) (7), 611 - 618, English

  [Refereed]

  Scientific journal


• Crystallization and preliminary X-ray analysis of LC3-I

  K Sugawara, NN Suzuki, Y Fujioka, N Mizushima, Y Ohsumi, F Inagaki

  Lead, Aug. 2003, ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY, 59(Pt 8) (Pt 8), 1464 - 1465, English

  [Refereed]

  Scientific journal

• 各種血糖降下薬 (インスリン以外) の作用, 使用上の注意など (7) イメグリミン

  菅原健二, 小川渉

  83 (増刊号3), 136-140,, 2025


• 糖尿病最新の治療2019-2021

  菅原健二, 小川渉

  Contributor, ビグアナイド薬, 南江堂, 2019


• DIABETES UPDATE 7巻2号

  菅原 健二, 小川渉

  Contributor, 最新論文レビューメトホルミンは未治療2型糖尿病患者の腸内細菌叢を変化させ、治療効果に寄与する。, メディカルレビュー社, May 2018


• 糖尿病学

  菅原健二, 清野進

  Contributor, インスリン分泌, 西村書店, May 2015


• Diabetes Frontier 25巻5号

  菅原健二, 清野進

  Contributor, インスリン分泌促進薬の作用メカニズム, メディカルレビュー社, Oct. 2014


• 成人病と生活習慣病 42巻12号

  菅原健二, 清野進

  Contributor, インスリン分泌の生理学、インスリン分泌のStimulatorとAmplifier, 東京医学社, Dec. 2012


• 臨床雑誌『内科』108巻4号

  菅原 健二, 清野 裕

  Contributor, インクレチン時代の糖尿病学, 南江堂, Oct. 2011

• 運動による筋量増加における機械刺激感受性イオンチャネルPiezo1の機能解析

  井上 朋也, 平田 悠, 菅原 健二, 西垣 智子, 倉本 尚樹, 穂積 かおり, 野村 和弘, 小川 渉

  第39回日本糖尿病・肥満動物学会年次学術集会, Feb. 2026, Japanese, 名古屋, Japan, Domestic conference


• SIMPRESEARCH®を用いたReal World Data研究フィージビリティ評価の実践と研究DX基盤としての展開

  菅原 健二, 牧野 奈緒, 市川 大介

  日本臨床試験学会第17回学術集会総会 ランチョンセミナー6, Feb. 2026, Japanese, 神戸, Japan, Domestic conference

  [Invited]

  Invited oral presentation


• 肥満症を伴う2型糖尿病合併妊娠における妊娠初期から産後までの当院でのマネジメントについて

  天野 桃望, 山田 倫子, 穂積 かおり, 菅原 健二

  第62回日本糖尿病学会近畿地方会, Nov. 2025, Japanese, 大阪, Japan, Domestic conference


• モデル動物・培養細胞1 膵β細胞からのインスリン分泌におけるMyocyte-specific enhancer factor 2Dの役割

  吉田 舞, 菅原 健二, 小川 渉

  第40回日本糖尿病合併症学会, Nov. 2025, Japanese, 東京, Japan, Domestic conference

  Oral presentation


• 肝細胞のPiezo1活性化によるMASLD進展抑制効果の解析

  井上 朋也, 平田 悠, 野村 和弘, 細川 友誠, 西垣 智子, 穂積 かおり, 菅原 健二, 小川 渉

  第46回日本肥満学会・第43回日本肥満症治療学会学術集会, Oct. 2025, Japanese, 岡山, Japan, Domestic conference

  Oral presentation


• 公開RNA-seqデータのメタ解析およびメンデルランダム化解析による健康アウトカムに関連する運動依存性遺伝子の探索

  井上 誠也, 菅原 健二, 井上 朋也, 小川 渉

  第25回日本糖尿病インフォマティクス学会年次学術集会, Aug. 2025, Japanese, 佐賀, Japan, Domestic conference

  Oral presentation


• 運動による筋量増加における機械刺激感受性イオンチャネルPiezo1の機能解析

  井上 朋也, 平田 悠, 野村 和弘, 菅原 健二, 西垣 智子, 倉本 尚樹, 穂積 かおり, 小川 渉

  第11回日本筋学会学術総会, Aug. 2025, Japanese, 宮城, Japan, Domestic conference


• Similarities and Differences in the Intestinal Actions of Metformin and Imeglimin

  Kenji Sugawara

  2025 Symposium on Adipose Regulation and Metabolism (Hohhot, China), Jul. 2025

  [Invited]


• イメグリミンとDPP-4阻害薬の併用が血糖マネジメントの改善につながったMODY3の一例

  高吉 倫史, 菅原 健二, 木戸 希, 齋藤 修一郎, 中辻 萌, 西影 星二, 芳村 魁, 山本 あかね, 小川 渉, 廣田 勇士

  第30回日本小児・思春期糖尿病学会年次学術集会, Jul. 2025, Japanese, 東京, Japan, Domestic conference

  Oral presentation


• 運動による筋量増加における機械刺激感受性イオンチャネルPiezo1の機能解析

  井上 朋也, 平田 悠, 野村 和弘, 菅原 健二, 西垣 智子, 倉本 尚樹, 穂積 かおり, 小川 渉

  第98回日本内分泌学会学術総会, Jun. 2025, Japanese, 千葉, Japan, Domestic conference


• インスリンアナログ製剤の違いによるアミロイド形成の要因と特性解析

  芳村 魁, 廣田 勇士, 菅原 健二, 齋藤 修一郎, 西影 星二, 山本 あかね, 高吉 倫史, 畠山 義清, 小川 渉

  第68回日本糖尿病学会年次学術集会, May 2025, Japanese, 岡山, Japan, Domestic conference

  Oral presentation


• 膵β細胞からのインスリン分泌におけるMyocyte-specific enhancer factor 2Dの役割

  吉田 舞, 菅原 健二, 小川 渉

  第68回日本糖尿病学会年次学術集会, May 2025, Japanese, 岡山, Japan, Domestic conference

  Oral presentation


• 1細胞RNA-Seq解析によるメトホルミンとイメグリミンの腸管作用の検討

  穂積かおり, 菅原健二, 平田悠, 小川渉

  第68回日本糖尿病学会年次学術集会, May 2025, Japanese, 岡山, Japan, Domestic conference

  Oral presentation


• メトホルミンが遷移金属の生体動態に及ぼす検討

  末松 那都, 坂口 一彦, 西坂 まり華, 福満 隼人, 桂 由佳梨, 森田 靖子, 山田 倫子, 菅原 健二, 岡田 裕子, 廣田 勇士, 小川 渉

  第68回日本糖尿病学会年次学術集会, May 2025, Japanese, 岡山, Japan, Domestic conference

  Oral presentation


• 公開データベースを用いたin silico解析による運動依存性新規経路探索の試み

  井上 朋也, 菅原 健二, 平田 悠, 野村 和弘, 西垣 智子, 小川 渉

  第68回日本糖尿病学会年次学術集会, May 2025, Japanese, 岡山, Japan, Domestic conference

  Oral presentation


• イメグリミンの膵外作用の基礎的検討～肝・腸管作用を中心に～

  菅原健二

  第68回日本糖尿病学会年次学術集会 シンポジウム15, May 2025

  [Invited]


• 若年発症糖尿病におけるHNF1A新規変異の同定と変異体3次元構造からの発症機序の解析

  原田 紗巴子, 菅原 健二, 高吉 倫史, 木戸 希, 廣田 勇士, 小川 渉

  医学生・研修医・専攻医の日本内科学会ことはじめ2025大阪, Apr. 2025, Japanese, 大阪, Japan, Domestic conference

  Oral presentation


• 運動による筋量増加における機械刺激感受性イオンチャネルPiezo1の機能解析

  井上 朋也, 平田 悠, 野村 和弘, 菅原 健二, 西垣 智子, 倉本 尚樹, 穂積 かおり, 小川 渉

  第60回日本臨床分子医学会学術集会, Apr. 2025, Japanese, 大阪, Japan, Domestic conference

  Oral presentation


• Metformin Treatment Is Associated with a Decrease in Serum Copper and Iron Levels in Individuals with Type 2 Diabetes

  Yamada T, Otowa-Suematsu N, Nishisaka M, Morita Y, Fukumitsu H, Katsura Y, Sugawara K, Okada Y, Hirota Y, Sakaguchi K, Ogawa W

  AASD2025, Mar. 2025, English, Taiwan, Taiwan, Province of China, International conference

  Poster presentation


• Myofiber Piezo1 regulates muscle hypertrophy and metabolism in response to exercise

  Inoue T, Hirata Y, Nomura K, Kuramoto N, Nishigaki T, Hozumi K, Sugawara K, Ogawa W

  17th Scientific Meeting of the Asian Association for the Study of Diabetes, Mar. 2025, English, Taiwan, Taiwan, Province of China, International conference

  Oral presentation


• 運動における機械刺激感受性イオンチャネルPiezo1を介した筋肥大、代謝制御機構の解明

  井上 朋也, 平田 悠, 野村 和弘, 倉本 尚樹, 西垣 智子, 穂積 かおり, 菅原 健二, 小川 渉

  第35回分子糖尿病学シンポジウム, Dec. 2024, Japanese, 熊本, Japan, Domestic conference

  Oral presentation


• 免疫チェックポイント阻害薬による1型糖尿病に対する当院での取り組み

  宮崎 裕也, 齋藤 修一郎, 菅原 健二, 廣田 勇士, 小川 渉, みやざき

  第61回日本糖尿病学会近畿地方会, Oct. 2024, Japanese, 大阪, Japan, Domestic conference

  Oral presentation


• Myofiber Piezo1 regulates muscle hypertrophy and metabolism in response to exercise

  T. Inoue, Y. Hirata, K. Nomura, N. Kuramoto, T. Nishigaki, K, Hozumi, K. Sugawara, W. Ogawa

  60th EASD Annual Meeting of the European Association for the Study of Diabetes (Madrid, Spain), Sep. 2024


• 糖代謝制御機構における消化管グルコース排泄の意義についての解析

  森田 靖子, 坂口 一彦, 野上 宗伸, 曽 菲比, 西坂 まり華, 末松 那都, 山田 倫子, 細川 友誠, 菅原 健二, 廣田 勇士, 村上 卓道, 小川 渉

  第67回日本糖尿病学会年次学術集会, May 2024, Japanese, 東京, Japan, Domestic conference


• The role of gut-muscle interaction in muscle mass regulation

  穂積 かおり, 平田 悠, 菅原 健二, 内山 奏, 井上 朋也, 安 立原, 西垣 智子, 野村 和弘, 小川 渉

  第67回日本糖尿病学会年次学術集会, May 2024, English, 東京, Japan, Domestic conference

  Nominated symposium


• Metformin prevents immobilization-induced muscle atrophy via intestinal actions

  Hozumi K, Sugawara K, Hirata Y, Nomura K, Nishigaki T, Ogawa W

  Cell Symposia: Exercise Metabolism, May 2024, English, Lisbon, Portugal, International conference

  Poster presentation


• The role of gut-muscle interaction in muscle mass regulation

  Hozumi K, Hirata Y, Sugawara K, Ogawa W

  Seoul Symposium on Obesity and Diabetes, Apr. 2024, English, Seoul, Korea, Republic of, International conference

  Oral presentation


• メトホルミンに調節される腸管腔へのグルコース排泄

  小川渉, 森田靖子, 細川友誠, 菅原健二, 坂口一彦

  第67回日本糖尿病学会年次学術集会, Apr. 2024, Japanese, Japan, Domestic conference


• Similarity and difference of intestinal actions of metformin and imeglimin

  Sugawara K, Mizuma H, Sasaki D, Kondo A, Watanabe Y, Ogawa W

  59th EASD Annual Meeting (Hamburg, Germany)


• Effects of Imeglimin on Mitochondrial Function, AMPK Activation, and Gene Expression in Hepatocytes and Myocytes

  Hozumi K, Sugawara K, Hirata Y, Nomura K, Ogawa W

  The 50th European Muscle Conference, Sep. 2023, English, Florence, Italy, International conference

  Poster presentation


• Quantitative analysis of metformin-induced glucose excretion in the intestine

  Hosokawa Y, Sakaguchi K, Ito J, Morita Y, Sugawara K, Ogawa W

  The 83rd American Diabetes Association Scientific Sessions, Jun. 2023, English, San Diego, United States, International conference

  Poster presentation


• The effects of imeglimin on incretin secretion

  権 映月, 菅原 健二, 高橋 晴美, 横井 伯英, 大林 健人, 岩崎 有作, 清野 進, 小川 渉

  第66回日本糖尿病学会年次学術集会, May 2023, English, 鹿児島, Japan, Domestic conference

  Oral presentation


• 肥満は腸管内腔グルコース排泄を増強する

  森田 靖子, 坂口 一彦, 野上 宗伸, 曽 菲比, 西坂 まり華, 伊藤 潤, 金子 景弘, 末松 那都, 山田 倫子, 菅原 健二, 廣田 勇士, 村上 卓道, 小川 渉

  第66回日本糖尿病学会年次学術集会, May 2023, Japanese, 鹿児島, Japan, Domestic conference

  Oral presentation


• 肝細胞におけるイメグリミンのミトコンドリア機能、AMPK活性化、遺伝子発現における効果

  穂積かおり, 菅原健二, 石原孝也, 石原直忠, 小川渉

  第58回日本臨床分子医学会学術集会, Apr. 2023, Japanese, 東京, Japan, Domestic conference

  Poster presentation


• 新規FDG-PET/MRI撮像法の開発によるメトホルミンの消化管ブドウ糖排泄作用の定量的分析

  伊藤 潤, 坂口 一彦, 野上 宗伸, 金子 景弘, 森田 靖子, 山田 倫子, 駒田 久子, 菅原 健二, 廣田 勇士, 小川 渉

  第95回日本内分泌学会学術総会, Jun. 2022, Japanese, 別府, Japan, Domestic conference

  Oral presentation


• 肝臓におけるイメグリミンとメトホルミンの作用の類似性と相違性

  穂積かおり, 菅原健二, 石原孝也, 石原直忠, 小川渉

  第95回日本内分泌学学会学術総会, Jun. 2022, Japanese, 別府, Japan, Domestic conference

  Oral presentation


• 新規FDG-PET/MRI撮像法の開発によるメトホルミン服用者における腸管ブドウ糖排泄の定量的解析

  伊藤 潤, 坂口 一彦, 野上 宗伸, 金子 景弘, 森田 靖子, 山田 倫子, 駒田 久子, 菅原 健二, 廣田 勇士, 小川 渉

  第65回日本糖尿病学会年次学術集会, May 2022, Japanese, 神戸, Japan, Domestic conference

  Oral presentation


• 耐糖能の変遷を長期間観察し得た反応性低血糖を呈するA型インスリン抵抗症の1例

  芳村 魁, 廣田 勇士, 西影 星二, 上田 真莉子, 山本 あかね, 高吉 倫史, 竹内 健人, 中川 靖, 浜口 哲矢, 菅原 健二, 小川 渉

  第65回日本糖尿病学会年次学術集会, May 2022, Japanese, 神戸, Japan, Domestic conference

  Oral presentation


• PET-MRI連続撮像法によるメトホルミン依存性腸管FDG排泄動態の解析

  森田 靖子, 坂口 一彦, 野上 宗伸, 伊藤 潤, 金子 景弘, 山田 倫子, 駒田 久子, 菅原 健二, 廣田 勇士, 小川 渉

  第65回日本糖尿病学会年次学術集会, May 2022, Japanese, 神戸, Japan, Domestic conference

  Oral presentation


• 肝臓におけるイメグリミンとメトホルミンの作用の類似性と相違性

  穂積かおり, 菅原健二, 石原孝也, 石原直忠, 小川渉

  第65回日本糖尿病学会年次学術集会, May 2022, Japanese, 神戸, Japan, Domestic conference

  Oral presentation


• HNF1AとNEUROD1の変異を認めた若年発症糖尿病の1例

  高吉 倫史, 廣田 勇士, 竹内 健人, 芳村 魁, 西影 星二, 浜口 哲矢, 菅原 健二, 高岡 裕, 佐竹 渉, 小川 渉

  第65回日本糖尿病学会年次学術集会, May 2022, Japanese, 神戸, Japan, Domestic conference

  Oral presentation


• PET-MRI連続撮像法によるメトホルミン依存性腸管FDG排泄動態の解析

  森田靖子, 野上宗伸, 坂口一彦, 伊藤潤, 金子景弘, 山田倫子, 駒田久子, 菅原健二, 廣田勇士, 村上卓道, 小川渉

  第42回日本肥満学会・第39回日本肥満症治療学会学術集会, Mar. 2022, Japanese, 横浜, Japan, Domestic conference

  Nominated symposium


• 新規PET-MRI撮像法の開発によるメトホルミンによる腸管FDG集積の解析

  伊藤潤, 野上宗伸, 坂口一彦, 金子景弘, 森田靖子, 山田倫子, 駒田久子, 菅原健二, 廣田勇士, 村上卓道, 小川渉

  第42回日本肥満学会, Mar. 2022, Japanese, Japan, Domestic conference


• Enhanced Release of Glucose into the Intraluminal Space of the Intestine Associated with Metformin Treatment as Revealed by 18F FDG-Based PET-MRI

  Kazuhiko Sakaguchi, Yasuko Morita, Munenobu Nogami, Yuko Okada, Yushi Hirota, Kenji Sugawara, Yoshikazu Tamori, Feibi Zeng, Takamichi Murakami, Wataru Ogawa

  American Diabetes Association -80th Scientific Sessions, Jun. 2020, English, Chicago (Online), United States, International conference

  Poster presentation


• 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

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


• 手術によって寛解後30年目に再発を認めた Cushing病の一例

  瀬尾 あかね, 福岡 秀規, 吉田 健一, 小原 靖子, 苛原 彩, 中野 温子, 藤原 えり, 坂本 洋一, 菅原 健二, 岡田 裕子, 廣田 勇士, 井口 元三, 小川 渉, 高橋 裕

  第27回臨床内分泌代謝Update, Nov. 2017, Japanese, 神戸, Japan, Domestic conference

  Poster presentation


• 1型糖尿病合併妊娠におけるCSIIとSensor Augmented Pump(SAP)療法のインスリン必要量の変化についての検討

  坂本 洋一, 岡田 裕子, 山田 倫子, 西本 祐希, 苛原 彩, 小原 靖子, 瀬尾 あかね, 中野 温子, 藤原 えり, 菅原 健二, 福岡 秀規, 廣田 勇士, 坂口 一彦, 小川 渉

  第34回日本糖尿病・妊娠学会年次学術集会, Nov. 2017, Japanese, 横浜, Japan, Domestic conference


• Chronic arsenic exposure impairs pancreatic beta cell function.

  Carmean CM, Kirkley AG, Yokoi N, Hoshikawa R, Sugawara K, Sargis RM, Seino S

  Society of Environmental Toxicology and Chemistry Conference (Brussel, Belgium), Nov. 2017


• 持効型インスリンが不要となったインスリン抗体陽性1型糖尿病の1例

  苛原 彩, 岡田 裕子, 坂本 洋一, 菅原 健二, 福岡 秀規, 廣田 勇士, 坂口 一彦, 小川 渉

  第54回日本糖尿病学会近畿地方会, Nov. 2017, Japanese, 大阪, Japan, Domestic conference


• インスリン分泌不全を基盤としてケトーシス発症し、MODY5の診断に至った一卵性双生児の例

  小原 靖子, 山田 倫子, 岡田 裕子, 坂本 洋一, 菅原 健二, 福岡 秀規

  第54回日本糖尿病学会近畿地方会, Nov. 2017, Japanese, 大阪, Japan, Domestic conference


• 新規変異型HNF4AによるMODY1の症例

  菅原健二, 岡田裕子, 坂本洋一, 廣田勇士, 坂口一彦, 松本真明, 粟野宏之, 菅野亜紀, 高岡裕, 小川渉

  第54回日本糖尿病学会近畿地方会, Nov. 2017, Japanese, Japan, Domestic conference


• 持効型インスリンが不要となった１型糖尿病の一例

  苛原 彩, 岡田 裕子, 坂本 洋一, 菅原 健二, 福岡 秀規, 廣田 勇士, 坂口 一彦, 小川 渉

  第15回1型糖尿病研究会, Nov. 2017, Japanese, 岩手, Japan, Domestic conference


• 1型糖尿病合併妊娠におけるCSIIとSensor Augmented Pump(SAP)療法のインスリン必要量の変化についての検討

  坂本 洋一, 岡田 裕子, 山田 倫子, 西本 祐希, 岩橋 泰幸, 村前 直和, 菅原 健二, 中村 友昭, 福岡 秀規, 廣田 勇士, 坂口 一彦, 小川 渉

  第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Japan, Domestic conference

  Oral presentation


• インスリン治療中の2型糖尿病患者におけるSGLT2阻害薬投与によるインスリン減量効果についての検討

  岩橋 泰幸, 岡田 裕子, 坂本 洋一, 村前 直和, 山田 倫子, 菅原 健二, 中村 友昭, 福岡 秀規, 廣田 勇士, 坂口 一彦, 小川 渉

  第60回日本糖尿病学会年次学術集会, May 2017, Japanese, 名古屋, Japan, Domestic conference

  Poster presentation


• Chronic arsenic exposure impairs pancreatic beta cell function.

  Carmean CM, Kirkley AG, Yokoi N, Hoshikawa R, Sugawara K, Sargis RM, Seino S

  The 9th Scientific Meeting of Asian Association for the Study of Diabetes (Nagoya, Japan), May 2017


• マイクロアレイ解析による、インスリノーマの分泌特性を規定する遺伝子発現量の検討

  菅原健二, 岡田裕子, 松田友和, 坂本洋一, 岩橋泰幸, 村前直和, 山田倫子, 中村友昭, 福岡秀規, 廣田勇士, 坂口一彦, 小川渉

  第60回日本糖尿病学会年次学術集会, May 2017, Japanese, Japan, Domestic conference


• Approaches to identification of novel small molecules that can be insulin secretagogues.

  Takahashi H, Sugawara K, Honda K, Yokoi N, Mori I, Nakaya H, Seino S

  2nd Joint Meeting of the EASD Islet Study Group & Beta Cell Workshop, May 2017

  [Invited]


• 周期性が疑われた嗅神経芽細胞腫による異所性ACTH症候群の一例

  金谷 雅之, 福岡 秀規, 菅原 健二, 岡田 裕子, 井口 元三, 小川 渉, 高橋 裕

  第90回日本内分泌学会学術総会, Apr. 2017, Japanese, 京都, Japan, Domestic conference

  Oral presentation


• 低K、低アルドステロン血症、低身長を呈した 若年性高血圧の一例

  細川 友誠, 福岡 秀規, 菅原 健二, 竹内 健人, 山田 倫子, 中村 友昭, 岡田 裕子, 廣田 勇士, 井口 元三, 本間 桂子, 長谷川 奉延, 小川 渉, 高橋 裕

  第26回臨床内分泌代謝Update, Nov. 2016, Japanese, 大宮, Japan, Domestic conference

  Poster presentation


• 性同一性障害を伴うコルチゾール、アンドロゲン産生腫瘍の1例

  岩橋 泰幸, 福岡 秀規, 毛利 華奈子, 菅原 健二, 岡田 裕子, 井口 元三, 小川 渉, 高橋 裕

  第26回臨床内分泌代謝Update, Nov. 2016, Japanese, 大宮, Japan, Domestic conference

  Poster presentation


• デュラグルチド導入後の血糖変動に与える短期効果についての検討

  平野 靖子, 村前 直和, 岡田 裕子, 立花 真莉子, 山田 倫子, 菅原 健二, 中村 友昭, 福岡 秀規, 廣田 勇士, 坂口 一彦, 小川 渉

  第53回日本糖尿病学会近畿地方会, Nov. 2016, Japanese, 大阪, Japan, Domestic conference

  Oral presentation


• SGLT2阻害薬導入後に著明な高グルカゴン血症を呈した一例

  金谷 雅之, 菅原 健二, 岡田 裕子, 岩橋 泰幸, 山田 倫子, 村前 直和, 中村 友昭, 福岡 秀規, 廣田 勇士, 坂口 一彦, 小川 渉

  第53回日本糖尿病学会近畿地方会, Nov. 2016, Japanese, 大阪, Japan, Domestic conference

  Oral presentation


• Trans-S-1-propenyl-l-cysteine sulfoxide from Allium cepa (onions) has appreciable antidiabetic potential in streptozotocin-induced diabetic mice

  Okechi OS, Sugawara K, Yoshida S, Takahashi H, Yokoi N, Nakayama M, Seino S

  The 11th IDF-WPR Congress and 8th AASD Scientific Meeting (Taipei, Taiwan), Oct. 2016


• Antidiabetic effect of trans-S-1-propenyl-L-cysteine sulfoxide from Allium cepa.

  Okechi OS, Sugawara K, Takahashi H, Yokoi N, Nakayama M, Seino S

  The 76th scientific sessions of the American Diabetes Association (New Orleans, USA), Jun. 2016


• Evaluation of the pharmacokinetics of a novel anti-diabetic agent using conventional LC/MS/MS.

  Sugawara K, Yokoi N, Hoshikawa R, Matsubara T, Seino S

  The 64th ASMS Conference on Mass Spectrometry and Allied Topics (San Antonio, USA), Jun. 2016


• KATPチャネルを標的とした新規低分子化合物の同定とその特性解析

  菅原健二, 本田洸平, 霊園良恵, 松本明郎, 森一郎, 中谷晴昭, 清野進

  第59回日本糖尿病学会年次学術集会, May 2016, Japanese, Japan, Domestic conference


• Chronic Arsenic Exposure Impairs Pancreatic Function.

  Carmean CM, Kirkley AG, Yokoi N, Hoshikawa R, Honda K, Gheni G, Sugawara K, Takahashi H, Sargis RM, Seino S

  17th International Group on Insulin Secretion Conference (Nice, France), Apr. 2016


• Identification of a novel small molecule targeting KATP channels to stimulate insulin secretion.

  Sugawara K, Shibasaki T, Minami K, Matsumoto A, Seki C, Mori I, Nakaya H, Seino S

  16th International Group on Insulin Secretion (Nice, France), Apr. 2015

  [Invited]


• Sulfonylurea act as an enhancer of Epac2 activation in cAMP-induced insulin secretion.

  Takahashi T, Shibasaki T, Takahashi H, Sugawara K, Seino S

  The 73th scientific sessions of the American Diabetes Association (Chicago, USA)., Jun. 2013


• Identification and characterization of the binding site and properties of antidiabetic sulfonylurea drugs in the cAMP sensor Epac2A.

  Takahashi T, Shibasaki T, Takahashi H, Sugawara K, Ono A, Seino S

  Beta Cell Workshop 2013 (Kyoto, Japan), Apr. 2013

  [Invited]


• Metformin enhances secretion of GLP-1 but not GIP and improves beta-cell function in Japanese patients with type 2 diabetes

  H Kuwata, D Yabe, K Sugawara, R Usui, K Sugizaki, Y Kitamoto, S Fujiwara, K Watanabe, T Hyo, T Murakami, T Yamaguchi, S Shimizu, H Eto, T Kurose, Y Seino

  8th Beta Cell Workshop, 2013, English, Kyoto, Japan, International conference


• GAD抗体高値を示しながらインスリン分泌能の保持が継続されている橋本病合併の1型糖尿病の1例

  桜町惟, 表孝徳, 臼井亮太, 菅原健二, 杉崎和, 桑田仁司, 藤原周一, 渡邊好胤, 安原章浩, 矢部大介, 黒瀬健, 清野裕

  第6回糖尿病臨床フォーラム, Mar. 2012, Japanese, 大阪, Japan, Domestic conference


• 意識障害で救急搬送された1型糖尿病ケトアシドーシスの1例

  小正晃裕, 表孝徳, 臼井亮太, 菅原健二, 杉本秀生, 杉崎和, 桑田仁司, 藤原周一, 渡邊好胤, 安原章浩, 矢部大介, 黒瀬健, 清野裕

  第6回糖尿病臨床フォーラム, Mar. 2012, Japanese, 大阪, Japan, Domestic conference


• ステロイド治療中にケトーシスを発症した多発性硬化症患者の一例

  倉本尚樹, 表孝徳, 臼井亮太, 菅原健二, 北村陽介, 杉崎和, 桑田仁司, 藤原周一, 渡邊好胤, 安原章浩, 矢部大介, 黒瀬健, 清野裕

  第6回糖尿病臨床フォーラム, Mar. 2012, Japanese, 大阪, Japan, Domestic conference


• Dietary intake and serum level of n-3 polyunsaturated fatty acids as predictors of DPP-4 inhibitor efficacy in patients with type 2 diabetes

  M. Iwasaki, D. Yabe, F. Hoshian, T. Tsuji, N. Hirose, T. Matsumoto, N. Kitatani, K. Sugawara, R. Usui, H. Kuwata, S. Fujiwara, K. Watanabe, T. Hyo, T. Kurose, Y. Seino

  47th EASD2012, Poster, 2012, English, Berlin, Germany, Germany, International conference

  Poster presentation


• Early detection of diabetic vascular complication using flow-mediated dilation (FMD) in patients with diabetes mellitus

  Koin Watanabe, Takeshi Kurose, Ryota Usui, Kenji Sugawara, Shuichi Fujiwara, Hitoshin Kuwata, Yuka Kitamoto, Kazu Sugizaki, Takanori Hyo, Mitsuo Fukushima, Daisuke Yabe, Yutaka Seino

  9th IDF-WPR Congress / 4th AASD Scientific Meeting, Oral, 2012, English, Kyoto, Japan, Japan, International conference

  Oral presentation


• Metformin Enhances Secretion of GLP-1 but not GIP and Ameliorates Postprandial Hyperglycemia in Japanese Type 2 Diabetes

  Hitoshi Kuwata, Daisuke Yabe, Kenji Sugawara, Ryota Usui, Kazu Sugizaki, Yuka Kitamoto, Shuichi Fujiwara, Koin Watanabe, Takanori Hyo, Takeshi Murakami, Takuro Yamaguchi, Shinobu Shimizu, Hiroaki Eto, Takeshi Kurose, Yutaka Seino

  9th IDF-WPR Congress / 4th AASD Scientific Meeting, Oral, 2012, English, Kyoto, Japan, Japan, International conference

  Oral presentation


• Metformin enhances secretion of GLP-1 but not GIP and improves postprandial glucose excursion in Japanese patients with type 2 diabetes

  H. Kuwata, D. Yabe, K. Sugawara, R. Usui, K. Sugizaki, Y. Kitamoto, S. Fujiwara, K. Watanabe, T. Hyo, T. Murakami, T. Yamaguchi, S. Shimizu, H. Eto, T. Kurose, Y. Seino

  47th EASD2012, Oral, 2012, English, Berlin, Germany, Germany, International conference

  Oral presentation


• Effects of Sitaglipptin, Acarbose and Sulfonylureas on Postprandial Levels of GLP-1 and GIP in Japanese Patients with Type 2 Diabetes

  Daisuke Yabe, Hitoshi Kuwabara, Koin Watanabe, Kenji Sugawara, Yuka Kitamoto, Sugizaki Kazu, Shuichi Fujiwara, Takanori Hyo, Kyoko Kuwabara, Kayo Yokota, Masahiro Iwasaki, Naomi Kitatani, Ryota Usui, Minori Matsumoto, Takeshi Kurose, Yutaka Seino

  9th IDF-WPR Congress / 4th AASD Scientific Meeting, Poster, 2012, English, Kyoto, Japan, Japan, International conference

  Poster presentation


• 瞳孔反応を用いた糖尿病神経障害の評価：糖尿病自律神経障害早期検出のためのカットオフ値の検討

  藤原周一, 矢部大介, 黒瀬健, 菅原健二, 臼井亮太, 北本友佳, 杉崎和, 桑田仁司, 渡邊好胤, 表孝徳, 清野裕

  第55回日本糖尿病学会年次学術集会, 2012, Japanese, 横浜, Japan, Domestic conference


• インスリンからリラグルチドへの変更時の効果および注意点に関する検討

  臼井亮太, 矢部大介, 菅原健二, 桑田仁司, 藤原周一, 北本友佳, 杉崎和, 渡邊好胤, 表孝徳, 安原章浩, 黒瀬健, 清野裕

  第55回日本糖尿病学会年次学術集会, 2012, Japanese, 横浜, Japan, Domestic conference


• 2型糖尿病患者におけるFMD値の検討について

  渡邊好胤, 黒瀬健, 菅原健二, 臼井亮太, 藤原周一, 北本友佳, 桑田仁司, 杉崎和, 表孝徳, 安原章浩, 矢部大介, 福島光夫, 清野裕

  第55回日本糖尿病学会年次学術集会, 2012, Japanese, 横浜, Japan, Domestic conference


• シタグリプチン投与時のSU薬とメトホルミンの影響

  桑田仁司, 臼井亮太, 菅原健二, 北本友佳, 杉崎和, 藤原周一, 渡邊好胤, 表孝徳, 安原章浩, 矢部大介, 黒瀬健, 清野裕

  第55回日本糖尿病学会年次学術集会, 2012, Japanese, 横浜, Japan, Domestic conference


• DPP-4阻害薬の血糖改善効果に影響する摂取および血中栄養素

  岩崎真宏, 矢部大介, 星庵史典, 辻とも子, 廣瀬直樹, 秋元知子, 北谷直美, 菅原健二, 臼井亮太, 桑田仁司, 杉崎和, 北本友佳, 渡邊好胤, 藤原周一, 表孝徳, 黒瀬健, 清野裕

  第55回日本糖尿病学会年次学術集会, 2012, Japanese, 横浜, Japan, Domestic conference


• 膵頭十二指腸切除術後の低栄養に消化酵素配合剤の投与が奏効した一例

  桑田仁司, 臼井亮太, 菅原健二, 北本友佳, 杉崎和, 藤原周一, 渡邊好胤, 表孝徳, 矢部大介, 安原章浩, 北谷直美, 黒瀬健, 清野裕

  第15回日本病態栄養学会年次学術集会, Jan. 2012, Japanese, 京都, Japan, Domestic conference


• インスリン開口分泌におけるRab11およびそのエフェクターRip11の役割

  菅原健二, 柴崎忠雄, 溝口明, 斉藤鉄也, 清野進

  第54回日本糖尿病学会年次学術集会, May 2011, Japanese, Japan, Domestic conference


• Efficacy and Safety of Insulin-to-Liraglutide Switch in Management of Type 2 Diabetes in Japanese

  Ryota Usui, Daisuke Yabe, Kenji Sugawara, Hitoshi Kuwata, Yuka Kitamoto, Kazu Sugizaki, Shuichi Fujiwara, Masahiro Hishizawa, Koin Watanabe, Takanori Hyo, Kayo Yokota, Masahiro Iwasaki, Naomi Kitatani, Takeshi Kurose, Yutaka Seino

  16th Japan-Korea Joint Symposium on Diabetes Mellitus, 2011, English, Tokyo, Japan, Korea, Republic of, International conference

  Nominated symposium


• Incretin Secretion in Japanese Patients with Type 2 Diabetes: Association with Clinical Parameters and Effects of Sulfonylureas

  Hitoshi Kuwata, Daisuke Yabe, Koin Watanabe, Masahiro Iwasaki, Kenji Sugawara, Ryota Usui, Yuka Kitamoto, Kazu Sugizaki, Shuichi Fujiwara, Masahiro Hishizawa, Takanori Hyo, Kayo Yokota, Naomi Kitatani, Takeshi Kurose, Yutaka Seino

  16th Japan-Korea Joint Symposium on Diabetes Mellitus, 2011, English, Tokyo, Japan, Korea, Republic of, International conference

  Nominated symposium


• Incretin Secretion in Japanese Patients with Type 2 Diabetes: Association with Clinical Parameters and Effects of Sulfonylureas

  H. Kuwata, D. Yabe, K. Watanabe, M. Iwasaki, K. Sugawara, R. Usui, R. Nakae, Y. Kitamoto, K. Sugizaki, S. Fujiwara, M. Hishizawa, T. Hyo, K. Kuwabara, K. Yokota, N. Kitatani, T. Kurose, Y. Seino

  3rd AASD Poster, 2011, English, Beijing, China, China, International conference

  Poster presentation


• Effects of sitagliptin, acarbose and sulfonylureas on postprandial levels of GLP-1 and GIP in Japanese patients with type 2 diabetes

  Daisuke Yabe, Koin Watanabe, Kenji Sugawara, Hitoshi Kuwata, Yuka Kitamoto, Kazu Sugisaki, Shuichi Fujiwara, Masahiro Hishizawa, Takanori Hyo, Kayo Yokota, Masahiro Iwasaki, Naomi Kitatani, Takeshi Kurose, Yutaka Seino

  47th EASD, 2011, English, Lisbon, Portugal, Portugal, International conference


• GIP Receptor Polymorphism rs10423928 and Glucagon Response after Glucose or Meal Ingestions

  D. Yabe, K. Watanabe, M. Iwasaki, K. Sugawara, R. Usui, H. Kuwata, R. Nakae, Y. Kitamoto, K. Sugizaki, S. Fujiwara, M. Hishizawa, T. Hyo, K. Kuwabara, K. Yokota, N. Kitatani, T. Kurose, Y. Seino

  3rd AASD Late Breaking Poster, 2011, English, Beijing, China, China, International conference

  Poster presentation


• 糖尿病患者におけるFMD測定値に関与する因子の検討

  黒瀬健, 杉崎和, 菅原健二, 桑田仁司, 藤原周一, 北本友佳, 臼井亮太, 渡邊好胤, 表孝徳, 矢部大介, 清野裕

  第48回日本糖尿病学会近畿地方会, 2011, Japanese, 大阪, Japan, Domestic conference


• 糖尿病を伴う胃癌患者における外科手術再建法の違いによる血糖コントロールへの影響についての検討

  表孝徳, 黒瀬健, 菅原健二, 桑田仁司, 藤原周一, 杉崎和, 北本友佳, 渡邊好胤, 矢部大介, 粟根雅章, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• 糖尿病ケトアシドーシス昏睡で発症した脳膿瘍の一例

  藤原周一, 表孝徳, 黒瀬健, 菅原健二, 北本友佳, 桑田仁司, 杉崎和, 渡邊好胤, 矢部大介, 清野裕

  第196回日本内科学会近畿地方会, 2011, Japanese, 京都, Japan, Domestic conference


• 糖尿病ケトアシドーシス昏睡で発症した脳膿瘍の一例

  藤原周一, 表孝徳, 黒瀬健, 臼井亮太, 菅原健二, 北本友佳, 杉崎和, 桑田仁司, 渡邊好胤, 矢部大介, 清野裕

  第48回日本糖尿病学会近畿地方会, 2011, Japanese, 大阪, Japan, Domestic conference


• 瞳孔反射を用いた糖尿病神経障害の評価：既存神経障害関連検査との相関とカットオフ値の検討

  藤原周一, 矢部大介, 菅原健二, 北本友佳, 杉崎和, 桑田仁司, 渡邊好胤, 表孝徳, 黒瀬健, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• インスリンからリラグルチドへの変更時の効果及び注意点に関する検討

  臼井亮太, 矢部大介, 菅原健二, 北本友佳, 桑田仁司, 杉崎和, 藤原周一, 渡邊好胤, 表孝徳, 黒瀬健, 清野裕

  第48回日本糖尿病学会近畿地方会, 2011, Japanese, 大阪, Japan, Domestic conference


• インスリンからリラグルチドへの治療変更に関する適応と有効性の検討

  矢部大介, 菅原健二, 桑田仁司, 北本友佳, 杉崎和, 藤原周一, 渡邊好胤, 表孝徳, 黒瀬健, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• 薬物未治療もしくは経口糖尿病薬治療中の2型糖尿病患者へのリラグルチド導入効果

  矢部大介, 臼井亮太, 菅原健二, 北本友佳, 杉崎和, 藤原周一, 渡邊好胤, 表孝徳, 安原章浩, 黒瀬健, 清野裕

  第48回日本糖尿病学会近畿地方会, 2011, Japanese, 大阪, Japan, Domestic conference


• シタグリプチン服用中に自己免疫性膵炎を発症した高齢2型糖尿病患者の1例

  渡邊好胤, 菅原健二, 表孝徳, 矢部大介, 東恵士朗, 染田仁, 黒瀬健, 中村武史, 清野裕

  第48回日本糖尿病学会近畿地方会, 2011, Japanese, 大阪, Japan, Domestic conference


• 当院における糖尿病地域連携パスを用いた患者の血糖コントロールの特徴について

  渡邊好胤, 矢部大介, 北谷直美, 菅原健二, 北本友佳, 桑田仁司, 杉崎和, 藤原周一, 菱澤方洋, 表孝徳, 黒瀬健, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• SU薬の併用がシタグリプチンの効果に変化を与えるか否かの検討

  桑田仁司, 黒瀬健, 杉崎和, 北本友佳, 菅原健二, 藤原周一, 表孝徳, 福島光夫, 北谷直美, 矢部大介, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• 日本人2型糖尿病患者のインクレチン分泌パターンの特徴と分泌に影響を与える因子の検索

  桑田仁司, 矢部大介, 臼井亮太, 菅原健二, 北本友佳, 杉崎和, 藤原周一, 渡邊好胤, 表孝徳, 黒瀬健, 清野裕

  第48回日本糖尿病学会近畿地方会, 2011, Japanese, 大阪, Japan, Domestic conference


• 糖尿病治療法選択時点における治療法と細小血管障害重症度との関連

  杉崎和, 黒瀬健, 菅原健二, 北本友佳, 桑田仁司, 藤原周一, 渡邊好胤, 菱澤方洋, 表孝徳, 矢部大介, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• リラグルチド導入による血糖日内変動の改善：持続血糖測定（CGM）と1,5-AGによる評価

  杉崎和, 矢部大介, 臼井亮太, 菅原健二, 北本友佳, 桑田仁司, 藤原周一, 渡邊好胤, 表孝徳, 黒瀬健, 清野裕

  第48回日本糖尿病学会近畿地方会, 2011, Japanese, 大阪, Japan, Domestic conference


• DPP-4阻害薬の血糖改善効果をより効果的にする食事療法

  岩崎真宏, 北谷直美, 矢部大介, 辻とも子, 渡邊好胤, 表孝徳, 北本友佳, 杉崎和, 桑田仁司, 藤原周一, 菅原健二, 黒瀬健, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• リラグルチド使用中の2型糖尿病患者の食事調査―リラグルチド開始前後の比較検討―

  北谷直美, 辻とも子, 岩崎真宏, 北本友佳, 杉崎和, 桑田仁司, 藤原周一, 菅原健二, 渡邊好胤, 表孝徳, 矢部大介, 黒瀬健, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• ペグインターフェロンによる慢性C型肝炎治療後に発症した1型糖尿病の一例

  北本友佳, 矢部大介, 菅原健二, 桑田仁司, 杉崎和, 藤原周一, 渡邊好胤, 表孝徳, 黒瀬健, 清野裕

  第48回日本糖尿病学会近畿地方会, 2011, Japanese, 大阪, Japan, Domestic conference


• 睡眠時無呼吸障害に関与する因子：肥満度及び血糖コントロールについて

  北本友佳, 矢部大介, 菅原健二, 桑田仁司, 杉崎和, 藤原周一, 渡邊好胤, 菱澤方洋, 表孝徳, 丸本圭一, 立花直子, 黒瀬健, 清野裕

  第54回日本糖尿病学会年次学術集会, 2011, Japanese, 札幌, Japan, Domestic conference


• Little enhancement of meal-induced GLP-1 secretion in Japanese: Comparison of type 2 diabetes and healthy controls.

  Sugawara K, Yabe D, Kuroe A, Lee S, Deacon CF, Watanabe K, Hyo T, Hishizawa M, Kurose T, Holst J.J, Hirano T, Inagaki N, Seino Y

  The 2nd Scientific Meeting of the Asian Association for the Study of Diabetes (Okayama, Japan), May 2010


• Impaired Super Early Insulin Phase Insulin Secretion and Its Genetic Restriction in Japanese

  Yuka Kitamoto, Daisuke Yabe, Koin Watanabe, Kazu Sugisaki, Iwao Okino, Kenji Sugawara, Masahiro Hisizawa, Takanori Hyo, Mitsuo Fukushima, Takeshi Kurose, Yutaka Seino

  Asia Islet Biology & Incretin Symposium, AIBIS 2010, 2010, English, Kyoto, Japan, International conference

  Nominated symposium


• No Enhancement of Meal-Induced GLP-1 Secretion and Reduced Intact GLP-1 Levels in Japanese: Comparison of Type 2 Diabetes and Healthy Controls

  Sugawara K, Yabe D, Kuroe A, Lee S, Deacon CF, Watanabe K, Hyo T, Hishizawa M, Kurose T, Hirano T, Holst JJ, Inagaki N, Seino Y

  8th IDF-WPR Congress Oral Presentation, 2010, English, Busan, Korea, Korea, Republic of, International conference

  Oral presentation


• Impaired super early phase insulin secretion and its genetic restriction in Japanese type 2 diabetes and controls

  Kitamoto Y, Yabe D, Watanabe K, Sugizaki K, Okino I, Sugawara K, Hishizawa M, Hyo T, Fukushima M, Kurose T, Seino Y

  2nd AASD Poster Session, 2010, English, Okayama, Japan, International conference

  Poster presentation


• Impaired Super Early Phase Insulin Secretion and Its Genetic Restriction in Japanese

  Kitamoto Y, Watanabe K, Sugizaki K, Okino I, Sugawara K, Hishizawa M, Hyo T, Fukushima M, Yabe D, Kurose T, Seino Y

  8th IDF-WPR Congress Oral Presentation, 2010, English, Busan, Korea, Korea, Republic of, International conference

  Oral presentation


• Evaluation of Plasma Thioredoxin and Glutathione Levels in Patients with Diabetes Mellitus

  Fujiwara S, Sugawara K, Sugizaki K, Kitamoto Y, Kuwata H, Watanabe K, Hishizawa M, Hyo T, Yabe D, Kurose T, Seino Y

  8th IDF-WPR Congress Oral Presentation, 2010, English, Busan, Korea, Korea, Republic of, International conference

  Oral presentation


• GIP receptor polymorphism rs10423928 affects body mass index and insulin and glucagon response after ingestion of glucose or mixed meals in Japanese

  D. Yabe, K. Watanabe, Y. Kitamoto, K. Sugisaki, K. Sugawara, M. Hishizawa, T. Hyo, T. Kurose, Y. Seino

  46th EASD, 2010, English, Stockholm, Sweden, International conference


• GAD抗体高値を示しながらインスリン分泌が保持された橋本病合併の1型糖尿病の一例

  表孝徳, 田中正代, 菅原健二, 桑田仁司, 藤原周一, 杉崎和, 北本友佳, 渡邊好胤, 矢部大介, 黒瀬健, 清野裕

  第47回日本糖尿病学会近畿地方会, 2010, Japanese, 大阪, Japan, Domestic conference


• シタグリプチン投与によりインスリン離脱が出来た糖尿病患者11例の検討

  藤原周一, 黒瀬健, 杉崎和, 北本友佳, 菅原健二, 桑田仁司, 渡邊好胤, 表孝徳, 福島光夫, 矢部大介, 清野裕

  第47回日本糖尿病学会近畿地方会, 2010, Japanese, 大阪, Japan, Domestic conference


• ヒト血漿中の活性型GLP-1濃度の測定法に関する検討

  矢部大介, 渡邊好胤, 沖野巌, 北本友佳, 杉崎和, 菅原健二, 菱澤方洋, 表孝徳, 橋本勉, 飯野由加里, 酒井千菜, 黒瀬健, 清野裕

  第53回日本糖尿病学会年次学術集会, 2010, Japanese, 岡山, Japan, Domestic conference


• 自己中断歴を有し糖尿病ケトアシドーシス（DKA）と肺炎球菌肺炎を合併した一例

  渡邊好胤, 北本友佳, 菅原健二, 杉崎和, 藤原周一, 桑田仁司, 表孝徳, 矢部大介, 黒瀬健, 清野裕

  第47回日本糖尿病学会近畿地方会, 2010, Japanese, 大阪, Japan, Domestic conference


• 糖尿病患者におけるシタグリプチン併用時の薬物減量の影響について

  桑田仁司, 黒瀬健, 杉崎和, 北本友佳, 菅原健二, 藤原周一, 渡邊好胤, 表孝徳, 福島光夫, 矢部大介, 清野裕

  第47回日本糖尿病学会近畿地方会, 2010, Japanese, 大阪, Japan, Domestic conference


• 糖尿病治療法選択時点における治療法と細小血管障害重傷度との関連

  杉崎和, 黒瀬健, 菅原健二, 北本友佳, 藤原周一, 桑田仁司, 渡邊好胤, 表孝徳, 矢部大介, 清野裕

  第25回日本糖尿病合併症学会, 2010, Japanese, 滋賀, Japan, Domestic conference


• 浮腫・貧血を契機に、低栄養を伴う著明な膵萎縮・慢性膵炎が判明した糖尿病の一例

  安田慎吾, 渡邊好胤, 菅原健二, 北本友佳, 杉崎和, 藤原周一, 桑田仁司, 表孝徳, 黒瀬健, 矢部大介, 清野裕

  第47回日本糖尿病学会近畿地方会, 2010, Japanese, 大阪, Japan, Domestic conference


• 日本人超早期インスリン分泌を規定する遺伝学的因子の検討

  北本友佳, 矢部大介, 渡辺好胤, 沖野巌, 杉崎和, 菅原健二, 菱澤方洋, 表孝徳, 大串美奈子, 大屋道洋, 黒瀬健, 清野裕

  第53回日本糖尿病学会年次学術集会, 2010, Japanese, 岡山, Japan, Domestic conference


• 口腔内感染症が敗血症の原因と考えられる2型糖尿病の一例

  北本友佳, 渡邊好胤, 矢部大介, 杉崎和, 沖野巌, 菅原健二, 菱澤方洋, 表孝徳, 福島光夫, 黒瀬健, 清野裕

  第47回日本糖尿病学会近畿地方会, 2010, Japanese, 大阪, Japan, Domestic conference


• 繰り返す事故中断によりインスリン依存状態に至った2型糖尿病患者の一例

  八木久美, 矢部大介, 菅原健二, 北本友佳, 桑田仁司, 杉崎和, 藤原周一, 渡邊好胤, 表孝徳, 黒瀬健, 清野裕

  第47回日本糖尿病学会近畿地方会, 2010, Japanese, 大阪, Japan, Domestic conference


• Evaluation of Oxidative Stress Biomarkers in Patients with Diabetes Mellitus

  Kitamoto Y, Kurose T, Hyo T, Sugawara K, Sugizaki K, Watanabe K, Hishizawa M, Fukushima M, Yabe D, Seino Y

  15th Korea-Japan Symposium on Diabetes Mellitus Symposium 9, 2009, English, Jeju, Korea, Korea, Republic of, International conference

  Nominated symposium


• グルカゴンの奇異性分泌亢進を認めた劇症1型糖尿病の一例

  菅原健二, 矢部大介, 渡邊好胤, 菱澤方洋, 表孝徳, 大屋道洋, 黒江彰, 大串美奈子, 奥正之, 黒瀬健, 清野裕

  第46回日本糖尿病学会近畿地方会, 2009, Japanese, 京都, Japan, Domestic conference


• 糖尿病地域連携パス：関西電力病院における取り組みと今後の課題

  矢部大介, 渡邊好胤, 菱澤方洋, 表孝徳, 北谷直美, 北本友佳, 杉崎和, 沖野巌, 菅原健二, 黒瀬健, 清野裕

  第46回日本糖尿病学会近畿地方会, 2009, Japanese, 京都, Japan, Domestic conference


• 日本人2型糖尿病における超早期インスリン分泌障害とグルカゴン分泌亢進

  沖野巌, 矢部大介, 菅原健二, 北本友佳, 杉崎和, 菱澤方洋, 渡邊好胤, 表孝徳, 黒瀬健, 清野裕

  第189回日本内科学会近畿地方会, 2009, Japanese, 大阪, Japan, Domestic conference


• 血中C-ペプチドと糖尿病細小血管障害との関連について

  杉崎和, 黒瀬健, 矢部大介, 北本友佳, 菅原健二, 渡邊好胤, 菱澤方洋, 表孝徳, 清野裕

  第46回日本糖尿病学会近畿地方会, 2009, Japanese, 京都, Japan, Domestic conference


• ミトコンドリアDNA3243変異を有するミトコンドリア糖尿病の一例

  北本友佳, 矢部大介, 渡邊好胤, 菱澤方洋, 表孝徳, 大屋道洋, 大串美奈子, 杉崎和, 菅原健二, 黒瀬健, 清野裕

  第46回日本糖尿病学会近畿地方会, 2009, Japanese, 京都, Japan, Domestic conference


• オートファジーに関する蛋白質LC3-Iの立体構造解析

  菅原健二, 鈴木展生, 藤岡優子, 水島昇, 大隅良典, 稲垣冬彦

  第3回日本蛋白質科学会年会, Jun. 2003, Japanese, Japan, Domestic conference

• THE JAPANESE SOCIETY OF INTERNAL MEDICINE


• The Japan Endocrine Society


• THE JAPAN DIABETES SOCIETY


• アジア糖尿病学会

• Analysis of the molecular mechanism of intestinal glucose excretion and its physiological significance.

  小川 渉, 坂口 一彦, 菅原 健二

  Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (A), Kobe University, 01 Apr. 2024 - 31 Mar. 2027


• 消化管における逆行性グルコース輸送機構の包括的解析

  公益財団法人木下記念事業団, 木下基礎科学研究基金助成事業, Jun. 2025 - May 2026, Principal investigator


• Elucidation of the molecular mechanism and physiological significance of retrograde glucose transport in the intestine.

  菅原 健二

  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


• メトホルミンが生体内の金属動態に与える影響およびその意義の解明

  鈴木万平糖尿病財団, 令和4年度 若手研究者調査研究助成, Oct. 2022 - Sep. 2024


• メトホルミンによる腸管腔内へのグルコース排泄機構の解明

  細胞科学研究財団, 令和３年度 研究助成, Apr. 2021 - Mar. 2024, Principal investigator


• 消化管における逆行性グルコース輸送機構の包括的解析

  第9回(2022年度)日本糖尿病財団・ベーリンガーインゲルハイム研究助成金, Dec. 2022 - Nov. 2023


• 鉄キレート作用を介したメトホルミンによる新規耐糖能改善メカニズムの解明

  菅原 健二

  Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C), Grant-in-Aid for Scientific Research (C), Kobe University, 01 Apr. 2020 - 31 Mar. 2023


• 腸管へのグルコース排泄による新規糖代謝制御機構の解明

  鈴木謙三記念医科学応用研究財団, 令和3年度調査研究助成, Dec. 2021 - Dec. 2022, Principal investigator


• 金属キレート作用を活用した抗糖尿病治療薬開発

  神戸医療産業都市研究開発助成金 若手支援枠, Sep. 2020 - Mar. 2022, Principal investigator


• 鉄キレート作用を介したメトホルミンの新規作用機序の解明

  菅原 健二

  MSD生命科学財団, 研究助成－生活習慣病領域－【若手研究者】, Dec. 2019, Principal investigator

  Competitive research funding


• 鉄キレート作用を介したメトホルミンによる新規耐糖能改善メカニズムの解明

  菅原 健二

  武田科学振興財団, 医学系研究助成, Aug. 2019, Principal investigator

  Competitive research funding


• ケミカルプロテオミクスによる新規インスリン分泌増強メカニズムの解明

  菅原 健二

  文部科学省, 科学研究費補助金(若手研究(B)), Apr. 2016 - Mar. 2019, Principal investigator

  Competitive research funding


• 新規糖尿病治療薬としてのEpac2A活性化化合物の同定

  菅原 健二

  日本糖尿病協会, 日本糖尿病協会若手研究者助成, Apr. 2015 - Mar. 2016, Principal investigator

  Competitive research funding


• 新規糖尿病治療薬としてのEpac2A活性化化合物の同定

  菅原 健二

  文部科学省, 科学研究費補助金(若手研究(B)), Apr. 2013 - Mar. 2016, Principal investigator

  Competitive research funding


• 新規糖尿病治療薬としてのEpac2A活性化化合物の同定

  菅原 健二

  日本糖尿病協会, 日本糖尿病協会若手研究者助成, Apr. 2014 - Mar. 2015, Principal investigator

  Competitive research funding

• 新規糖尿病治療剤

  清野 進, 菅原 健二, 森 一郎, 松本 明郎, 霊園 良恵

  特願2017-163122, 28 Aug. 2017, JCRファーマ株式会社, 国立大学法人神戸大学, 国立大学法人千葉大学, 特開2018-039795, 15 Mar. 2018

  Patent right

  IRI