The mechanism of recovery after inhibition of insulin receptor and IGF-1 receptor in pancreatic beta cells, liver, adipose tissue.

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K19542
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Metabolomics
• 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
• Keywords: インスリン抵抗性 / 膵β細胞 / 脂肪 / 脂肪肝

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.

Free Research Field

糖尿病