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SUGAWARA Kenji
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■ Award- 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
- 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 magazineScientific journal
- 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 magazineScientific journal
- 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 magazineScientific journal
- Japan Endocrine Society, 2025, Endocrine JournalScientific journal
- 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
- 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]
- 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
- 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
- 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
- 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
- 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
- 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
- Lead, Dec. 2019, Journal of Diabetes InvestigationRelation between metformin use and vitamin B12 status in patients with type 2 diabetes in Japan[Refereed]
- 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
- 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
- Sep. 2017, DIABETES OBESITY & METABOLISM, 19, 22 - 29, English[Refereed]
- Lead, Oct. 2016, PLOS ONE, 11(10) (10), e0164785, English[Refereed]Scientific journal
- Lead, Jan. 2016, GENE, 575(2) (2), 577 - 583, English[Refereed]
- Oct. 2014, CELL REPORTS, 9(2) (2), 661 - 673, English[Refereed]Scientific journal
- Oct. 2013, SCIENCE SIGNALING, 6(298) (298), ra94, English[Refereed]Scientific journal
- Oct. 2012, JOURNAL OF DIABETES INVESTIGATION, 3(5) (5), 464 - 467, English[Refereed]Scientific journal
- Feb. 2012, JOURNAL OF DIABETES INVESTIGATION, 3(1) (1), 70 - 79, English[Refereed]Scientific journal
- THE JAPAN DIABETES SOCIETY, 2012, Journal of the Japan Diabetes Society, 55(7) (7), 477 - 482, Japanese[Refereed]
- Lead, Apr. 2009, GENES TO CELLS, 14(4) (4), 445 - 456, English[Refereed]Scientific journal
- Lead, Dec. 2005, JOURNAL OF BIOLOGICAL CHEMISTRY, 280(48) (48), 40058 - 40065, English[Refereed]Scientific journal
- Lead, Jul. 2004, GENES TO CELLS, 9(7) (7), 611 - 618, English[Refereed]Scientific journal
- Lead, Aug. 2003, ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY, 59(Pt 8) (Pt 8), 1464 - 1465, English[Refereed]Scientific journal
- Dec. 2024, 第35回 分子糖尿病学シンポジウム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
- (一社)日本糖尿病学会, Apr. 2024, 糖尿病, 67(Suppl.1) (Suppl.1), S - 157, Japanese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
- (一社)日本糖尿病学会, Apr. 2024, 糖尿病, 67(Suppl.1) (Suppl.1), S - 33, English腸内環境とSugar:health and disease メトホルミンが制御する腸管内腔へのグルコース排出(Gut and sugar: health and disease Metformin-regulated glucose excretion into the intestinal lumen)
- (一社)日本糖尿病学会, Apr. 2024, 糖尿病, 67(Suppl.1) (Suppl.1), S - 59, Japanese骨格筋を中心とした組織間ネットワーク 腸管 骨格筋相互作用による筋量制御のメカニズム
- (公財)鈴木謙三記念医科学応用研究財団, Feb. 2024, 医科学応用研究財団研究報告, 41, 464 - 466, Japanese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
- 2024, 医科学応用研究財団研究報告(CD-ROM), 41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
- 日本臨床分子医学会, Apr. 2023, 日本臨床分子医学会学術総会プログラム・抄録集, 58回, 51 - 51, Japanese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
- (一社)日本糖尿病学会, Apr. 2023, 糖尿病, 66(Suppl.1) (Suppl.1), S - 177, Englishインクレチン分泌に対するimegliminの効果(The effects of imeglimin on incretin secretion)
- (一社)日本糖尿病学会, Apr. 2023, 糖尿病, 66(Suppl.1) (Suppl.1), S - 247, Japanese肥満は腸管内腔グルコース排泄を増強する
- 2023, 糖尿病(Web), 66(Suppl) (Suppl)肥満は腸管内腔グルコース排泄を増強する
- 2023, 糖尿病(Web), 66(Suppl) (Suppl)The effects of imeglimin on incretin secretion
- (一社)日本内分泌学会, Apr. 2022, 日本内分泌学会雑誌, 98(1) (1), 311 - 311, Japanese
- (一社)日本糖尿病学会, Apr. 2022, 糖尿病, 65(Suppl.1) (Suppl.1), S - 130, Japanese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
- (一社)日本糖尿病学会, Apr. 2022, 糖尿病, 65(Suppl.1) (Suppl.1), S - 152, Japanese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
- (一社)日本糖尿病学会, Apr. 2022, 糖尿病, 65(Suppl.1) (Suppl.1), S - 158, JapaneseHNF1AとNEUROD1の変異を認めた若年発症糖尿病の1例
- (一社)日本糖尿病学会, Apr. 2022, 糖尿病, 65(Suppl.1) (Suppl.1), S - 161, Japanese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
- (一社)日本糖尿病学会, Apr. 2022, 糖尿病, 65(Suppl.1) (Suppl.1), S - 163, JapanesePET/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
- (一社)日本肥満学会, Mar. 2022, 肥満研究, 27(Suppl.) (Suppl.), 166 - 166, Japanese減量効果を期待できる薬剤の現状と未来 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
- (一社)日本肥満学会, Mar. 2022, 肥満研究, 27(Suppl.) (Suppl.), 334 - 334, Japanese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
- 2022, 糖尿病(Web), 65(Suppl) (Suppl)HNF1AとNEUROD1の変異を認めた若年発症糖尿病の1例
- 2022, 糖尿病(Web), 65(Suppl) (Suppl)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
- (一社)日本内分泌学会, 2022, 日本内分泌学会雑誌, 98(1) (1), 310 - 310, Japanese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
- メディカルレビュー社, May 2019, Diabetes update = ダイアベーテスアップデート : frontiers in diabetes, 8(2) (2), 70 - 72, JapaneseMetformin inhibits gluconeogenesis via a redox-dependent mechanism in vivo
- (一社)日本糖尿病学会, Apr. 2019, 糖尿病, 62(Suppl.1) (Suppl.1), S - 313, Japanese新規インスリン分泌促進薬シード化合物の同定とその作用機序の解明
- (一社)日本糖尿病・妊娠学会, Mar. 2019, 糖尿病と妊娠, 19(1) (1), 28 - 36, Japanese1型糖尿病合併妊娠におけるContinuous subcutaneous insulin injection療法とSensor Augmented Pump療法のインスリン必要量の変化についての検討
- (一社)日本糖尿病学会, Jun. 2018, 糖尿病, 61(6) (6), 421 - 421, Japanese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
- (一社)日本糖尿病学会, Jun. 2018, 糖尿病, 61(6) (6), 455 - 455, Japanese新規変異型HNF4AによるMODY1の症例
- (一社)日本糖尿病学会, Jun. 2018, 糖尿病, 61(6) (6), 456 - 456, Japanese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
- (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61(Suppl.1) (Suppl.1), S - 147, Japanese糖尿病患者におけるビタミンD欠乏に関連する因子についての検討
- (一社)日本糖尿病学会, Apr. 2018, 糖尿病, 61(Suppl.1) (Suppl.1), S - 238, Japanese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
- 2018, 糖尿病(Web), 61(Suppl) (Suppl)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
- (一社)日本糖尿病・妊娠学会, Nov. 2017, 糖尿病と妊娠, 17(3) (3), S - 92, Japanese1型糖尿病合併妊娠におけるCSIIとSAP療法のインスリン必要量の変化についての検討
- (一社)日本内分泌学会, Oct. 2017, 日本内分泌学会雑誌, 93(2) (2), 599 - 599, Japanese手術によって寛解後30年目に再発を認めたCushing病の一例
- (一社)日本糖尿病学会, Sep. 2017, 糖尿病, 60(9) (9), 623 - 623, Japanese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
- (一社)日本糖尿病学会, Sep. 2017, 糖尿病, 60(9) (9), 627 - 627, JapaneseSGLT2阻害薬導入後に著明な高グルカゴン血症を呈した1例
- (一社)日本糖尿病学会, Apr. 2017, 糖尿病, 60(Suppl.1) (Suppl.1), S - 208, Japanese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
- (一社)日本糖尿病学会, Apr. 2017, 糖尿病, 60(Suppl.1) (Suppl.1), S - 406, Japaneseインスリン治療中の2型糖尿病患者におけるSGLT-2阻害薬投与によるインスリン減量効果についての検討
- (一社)日本内分泌学会, Oct. 2016, 日本内分泌学会雑誌, 92(2) (2), 475 - 475, Japanese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
- (一社)日本内分泌学会, Oct. 2016, 日本内分泌学会雑誌, 92(2) (2), 491 - 491, Japanese性同一性障を伴うコルチゾール、アンドロゲン産生副腎腫瘍の1例
- Oct. 2016, DIABETES RESEARCH AND CLINICAL PRACTICE, 120, S61 - S62, EnglishTrans-S-1-propenyl-l-cysteine sulfoxide from Allium cepa (onions) has appreciable antidiabetic potential in streptozotocin-induced diabetic miceSummary international conference
- Jun. 2016, DIABETES, 65, A616 - A616, EnglishAntidiabetic Effect of Trans-S-1-propenyl-L-cysteine Sulfoxide, from Allium CepaSummary international conference
- (一社)日本糖尿病学会, Apr. 2016, 糖尿病, 59(Suppl.1) (Suppl.1), S - 193, JapaneseKATP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
- 2016, 糖尿病(Web), 59(Suppl) (Suppl), S.193(J‐STAGE), JapaneseKATP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
- (株)メディカルレビュー社, Oct. 2014, Diabetes Frontier, 25(5) (5), 556 - 562, Japanese【インスリン分泌促進薬の現状と新たな展望】 インスリン分泌促進薬の作用メカニズム
- (公社)日本生化学会, Oct. 2014, 日本生化学会大会プログラム・講演要旨集, 87回, [3P - 022], Japaneseインスリン分泌増強効果を有する新規低分子化合物の同定とその特性解析
- (一社)日本糖尿病学会, Apr. 2014, 糖尿病, 57(Suppl.1) (Suppl.1), S - 256, Japaneseスルホニル尿素(SU)薬とcAMPの協調作用によるEpac2A活性化
- (一社)日本糖尿病学会, Apr. 2014, 糖尿病, 57(Suppl.1) (Suppl.1), S - 404, Japaneseインスリン分泌増強効果を有する新規低分子化合物の同定とその特性解析
- (株)東京医学社, Dec. 2013, 成人病と生活習慣病, 43(12) (12), 1439 - 1443, Japanese【インクレチン関連薬による糖尿病治療の新時代】 インスリン分泌の生理学 インスリン分泌のStimulatorとAmplifier
- (一社)日本糖尿病学会, Sep. 2012, 糖尿病, 55(9) (9), 727 - 727, Japanese糖尿病ケトアシドーシス昏睡で発症した脳膿瘍の1例
- (一社)日本糖尿病学会, Sep. 2012, 糖尿病, 55(9) (9), 730 - 730, Japanese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
- (一社)日本糖尿病学会, Sep. 2012, 糖尿病, 55(9) (9), 731 - 731, Japanese糖尿病患者におけるFMD測定値に関与する因子の検討
- (一社)日本糖尿病学会, Aug. 2012, 糖尿病, 55(8) (8), 647 - 647, Japanese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の効果
- (一社)日本糖尿病学会, Aug. 2012, 糖尿病, 55(8) (8), 649 - 649, Japanese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
- (一社)日本糖尿病学会, Aug. 2012, 糖尿病, 55(8) (8), 656 - 656, Japanese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
- (一社)日本糖尿病学会, Aug. 2012, 糖尿病, 55(8) (8), 657 - 657, Japanese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
- (一社)日本糖尿病学会, Aug. 2012, 糖尿病, 55(8) (8), 667 - 667, Japanese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1例
- (一社)日本糖尿病学会, Jul. 2012, 糖尿病, 55(7) (7), 477 - 482, Japanese
- (一社)日本糖尿病学会, Apr. 2012, 糖尿病, 55(Suppl.1) (Suppl.1), S - 95, Japanese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
- (一社)日本糖尿病学会, Apr. 2012, 糖尿病, 55(Suppl.1) (Suppl.1), S - 177, Japanese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
- (一社)日本糖尿病学会, Apr. 2012, 糖尿病, 55(Suppl.1) (Suppl.1), S - 256, Japaneseシタグリプチン投与時のSU薬とメトホルミンの影響
- (一社)日本糖尿病学会, Apr. 2012, 糖尿病, 55(Suppl.1) (Suppl.1), S - 306, JapaneseDPP-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
- (一社)日本糖尿病学会, Apr. 2012, 糖尿病, 55(Suppl.1) (Suppl.1), S - 318, Japanese2型糖尿病患者におけるFMD値の検討について
- 関西電力病院, Dec. 2011, 関西電力病院医学雑誌, (43) (43), 1 - 2, Japanese糖尿病患者と口腔ケア
- (株)南江堂, Oct. 2011, 内科, 108(4) (4), 567 - 573, Japanese【最新版 糖尿病虎の巻-新時代の糖尿病診療を実践する】 インクレチン時代の糖尿病学
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 110, Japanese睡眠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
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 123, Japanese瞳孔反応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
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 160, Japanese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
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 187, Japanese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
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 188, Japanese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
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 189, JapaneseDPP-4阻害薬の血糖改善効果をより効果的にする食事療法
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 239, JapaneseSU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
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 260, Japanese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
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 289, Japanese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
- (一社)日本糖尿病学会, Apr. 2011, 糖尿病, 54(Suppl.1) (Suppl.1), S - 291, Japanese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
- (一社)日本糖尿病学会, Mar. 2011, 糖尿病, 54(3) (3), 204 - 204, Japanese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
- (一社)日本糖尿病学会, Mar. 2011, 糖尿病, 54(3) (3), 207 - 207, Japanese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
- (一社)日本糖尿病学会, Mar. 2011, 糖尿病, 54(3) (3), 210 - 210, Japanese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
- (一社)日本糖尿病学会, Mar. 2011, 糖尿病, 54(3) (3), 211 - 211, Japanese繰り返す自己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
- (一社)日本糖尿病学会, Mar. 2011, 糖尿病, 54(3) (3), 214 - 214, Japanese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
- (一社)日本糖尿病学会, Mar. 2011, 糖尿病, 54(3) (3), 216 - 216, Japanese自己中断歴を有し糖尿病性ケトアシドーシス(DKA)と肺炎球菌性肺炎を合併した一例
- (一社)日本糖尿病学会, Mar. 2011, 糖尿病, 54(3) (3), 221 - 221, JapaneseGAD抗体高値を示しながらインスリン分泌能が保持された橋本病合併の1型糖尿病の一例
- 関西電力病院, Dec. 2010, 関西電力病院医学雑誌, (37,38,39,40,41,42合併号) (37,38,39,40,41,42合併号), 1 - 7, Japaneseインクレチン研究の歴史と臨床における治療応用
- (一社)日本糖尿病合併症学会, Oct. 2010, 糖尿病合併症, 24(Suppl.1) (Suppl.1), 103 - 103, Japanese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
- (一社)日本糖尿病学会, Apr. 2010, 糖尿病, 53(Suppl.1) (Suppl.1), S - 124, Japanese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
- (一社)日本糖尿病学会, Apr. 2010, 糖尿病, 53(Suppl.1) (Suppl.1), S - 177, Japanese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
- (一社)日本糖尿病学会, Apr. 2010, 糖尿病, 53(Suppl.1) (Suppl.1), S - 195, Japaneseヒト血漿中の活性型GLP-1濃度の測定法に関する検討
- (一社)日本糖尿病学会, Feb. 2010, 糖尿病, 53(2) (2), 119 - 119, Japanese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
- (一社)日本糖尿病学会, Feb. 2010, 糖尿病, 53(2) (2), 127 - 127, Japanese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
- (一社)日本糖尿病学会, Feb. 2010, 糖尿病, 53(2) (2), 148 - 148, Japanese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
- (一社)日本糖尿病学会, Feb. 2010, 糖尿病, 53(2) (2), 152 - 152, Japanese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
- Jun. 2003, 第3回日本蛋白質科学会年会オートファジーに関する蛋白質LC3-Iの立体構造解析
- Contributor, ビグアナイド薬, 南江堂, 2019糖尿病最新の治療2019-2021
- 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 2018DIABETES UPDATE 7巻2号
- Contributor, インスリン分泌, 西村書店, May 2015糖尿病学
- 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. 2014Diabetes Frontier 25巻5号
- 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成人病と生活習慣病 42巻12号
- Contributor, インクレチン時代の糖尿病学, 南江堂, Oct. 2011臨床雑誌『内科』108巻4号
- 60th EASD Annual Meeting of the European Association for the Study of Diabetes (Madrid, Spain), Sep. 2024Myofiber Piezo1 regulates muscle hypertrophy and metabolism in response to exercise
- 59th EASD Annual MeetingSimilarity and difference of intestinal actions of metformin and imeglimin
- The 50th European Muscle ConferenceEffects of Imeglimin on Mitochondrial Function, AMPK Activation, and Gene Expression in Hepatocytes and Myocytes
- The 83rd American Diabetes Association Scientific Sessions.Quantitative analysis of metformin-induced glucose excretion in the intestine
- Society of Environmental Toxicology and Chemistry Conference (Brussel, Belgium), Nov. 2017Chronic arsenic exposure impairs pancreatic beta cell function.
- The 9th Scientific Meeting of Asian Association for the Study of Diabetes (Nagoya, Japan), May 2017Chronic arsenic exposure impairs pancreatic beta cell function.
- 2nd Joint Meeting of the EASD Islet Study Group & Beta Cell Workshop, May 2017Approaches to identification of novel small molecules that can be insulin secretagogues.[Invited]
- The 11th IDF-WPR Congress and 8th AASD Scientific Meeting (Taipei, Taiwan), Oct. 2016Trans-S-1-propenyl-l-cysteine sulfoxide from Allium cepa (onions) has appreciable antidiabetic potential in streptozotocin-induced diabetic mice
- The 76th scientific sessions of the American Diabetes Association (New Orleans, USA), Jun. 2016Antidiabetic effect of trans-S-1-propenyl-L-cysteine sulfoxide from Allium cepa.
- The 64th ASMS Conference on Mass Spectrometry and Allied Topics (San Antonio, USA), Jun. 2016Evaluation of the pharmacokinetics of a novel anti-diabetic agent using conventional LC/MS/MS.
- 17th International Group on Insulin Secretion Conference (Nice, France), Apr. 2016Chronic Arsenic Exposure Impairs Pancreatic Function.
- 16th International Group on Insulin Secretion (Nice, France), Apr. 2015Identification of a novel small molecule targeting KATP channels to stimulate insulin secretion.[Invited]
- The 73th scientific sessions of the American Diabetes Association (Chicago, USA)., Jun. 2013Sulfonylurea act as an enhancer of Epac2 activation in cAMP-induced insulin secretion.
- Beta Cell Workshop 2013 (Kyoto, Japan), Apr. 2013Identification and characterization of the binding site and properties of antidiabetic sulfonylurea drugs in the cAMP sensor Epac2A.[Invited]
- The 2nd Scientific Meeting of the Asian Association for the Study of Diabetes (Okayama, Japan), May 2010Little enhancement of meal-induced GLP-1 secretion in Japanese: Comparison of type 2 diabetes and healthy controls.
- THE JAPANESE SOCIETY OF INTERNAL MEDICINE
- The Japan Endocrine Society
- THE JAPAN DIABETES SOCIETY
- アジア糖尿病学会
- 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. 2026Elucidation of the molecular mechanism and physiological significance of retrograde glucose transport in the intestine.
- 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
- 細胞科学研究財団, 令和3年度 研究助成, Apr. 2021 - Mar. 2024, Principal investigator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
- 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
- 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
- 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
- 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金属キレート作用を活用した抗糖尿病治療薬開発
- 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Competitive research funding
- 武田科学振興財団, 医学系研究助成, Aug. 2019, Principal investigator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Competitive research funding
- 文部科学省, 科学研究費補助金(若手研究(B)), Apr. 2016 - Mar. 2019, Principal investigator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Competitive research funding
- 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新規糖尿病治療薬としてのEpac2A活性化化合物の同定Competitive research funding
- 文部科学省, 科学研究費補助金(若手研究(B)), Apr. 2013 - Mar. 2016, Principal investigator新規糖尿病治療薬としてのEpac2A活性化化合物の同定Competitive research funding
- 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新規糖尿病治療薬としてのEpac2A活性化化合物の同定Competitive research funding