The mechanism of recovery after inhibition of insulin receptor and IGF-1 receptor in pancreatic beta cells, liver, adipose tissue.
Project/Area Number |
16K19542
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Metabolomics
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Research Institution | Yokohama City University |
Principal Investigator |
TOGASHI Yu 横浜市立大学, 附属病院, 助教 (10710444)
|
Research Collaborator |
TERAUCHI Yasuo
SHIRAKAWA Jun
TAJIMA Kazuki
ORIME Kazuki
OKUYAMA Tomoko
|
Project Period (FY) |
2016-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | インスリン抵抗性 / 膵β細胞 / 脂肪 / 脂肪肝 / 肝臓 |
Outline of Final Research Achievements |
Molecular mechanisms of plastic changes of pancreatic β cells, liver, adipose tissue under and after insulin resistance were analyzed using insulin receptor IGF-1 receptor blocker, OSI-906 administration model. OSI-906 administration showed pancreatic β-cell proliferation independent of insulin/IGF-1, significant atrophy of visceral fat, and fatty liver. These differences were not shown after withdrawal of OSI-906. In this model, administration of leptin, a drug for lipoatrophic diabetes, and DPP-4 inhibitor, an oral diabetes agent, improved fatty liver, and administration of SGLT-2 inhibitor, an oral diabetes agent, improved glucose tolerance. These results suggested that these agents have organ-specific effect independent of insulin/IGF-1.
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Report
(3 results)
Research Products
(3 results)