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2015 Fiscal Year Final Research Report

The mechanism of pancreatic beta cell proliferation after a pancreatectomy

Research Project

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Project/Area Number 26860698
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Metabolomics
Research InstitutionYokohama City University

Principal Investigator

TOGASHI YU  横浜市立大学, 医学部, 助教 (10710444)

Research Collaborator TERAUCHI Yasuo  
SHIRAKAWA Jun  
TAJIMA Kazuki  
ORIME Kazuki  
Project Period (FY) 2014-04-01 – 2016-03-31
Keywords膵β細胞
Outline of Final Research Achievements

We investigated panreatectomised wild-type and IRS-2-KO mice to larify the role of IRS-2 in pancreatic beta cells. IRS-2 mice showed hyperglycemia and hypoinsulinemia after a pancreatectomy(Px), and oral administration of hypoglycemic agents improved the insulin secretion.The inslulin secretion of isolated islets from Px IRS-2 mice were not impaired regardless of normalization of blood glucose levels. In addition, normalization of hyperglycemia in Px IRS-2 mice did not decrease the beta cell proliferation after a pancreatectomy in IRS-2 mice. These data suggests that the beta cell proliferation after a pancreatectomy is independent of insulin signal mediated IRS-2, or glucose signal,and that the function of regenerative beta cells have normal function.

Free Research Field

糖尿病学

URL: 

Published: 2017-05-10  

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