2016 Fiscal Year Final Research Report
Physiological role of pancreatic incretin on the functional regulation of pancreatic islet cells
Project/Area Number |
26461350
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Metabolomics
|
Research Institution | Kawasaki Medical School |
Principal Investigator |
Kaku Kohei 川崎医科大学, 医学部, 教授 (10116709)
|
Research Collaborator |
NAKASHIMA Koji
KIMURA Tomohiko
HIRUKAWA Hidenori
OKAUCHI Seizo
OBATA Atsushi
KANETO Hideaki
SHIGETO Makoto
Rorsman Patrik
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | 糖尿病 / 膵ラ氏島機能 / 膵灌流 / 膵インクレチン / 膵α細胞 / GLP-1 / GLP-1受容体 / autocrine作用 |
Outline of Final Research Achievements |
To assess a physiological role of pancreatic GLP-1 on the regulation of pancreatic islet cell function, GLP-1 secretion by using pancreas perfusion study and GLP-1 receptors (GLP-1Rs) in islet cells by immunohistochemical analysis were investigated in non-diabetic and diabetic rats. The perfusion study of diabetic GK rats demonstrated a significant secretion of GLP-1 from the pancreas. GLP-1Rs were observed in α-cells in diabetic GK rats, but not in non-diabetic rats. Exendin-4 stimulated both glucagon and GLP-1 secretions from α-cells and cAMP-dependent insulin secretion from β-cells. In addition, the immunostochemical analysis revealed that GLP-1/GLP-1R complex induced the endosome formation in pancreatic α-cells of diabetic rats. These results strongly suggested the existence of autocrine mechanism of GLP-1/GLP-1R in pancreatic α-cells of diabetic rats, by which the deranged islet function in diabetic condition might be restored.
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Free Research Field |
医歯薬学
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