Insulin secretion in pancreatic .BETA.-cells: role of protein palmitoylation in glucose-induced insulin secretion

Accession number;05A0630941
Title;Insulin secretion in pancreatic .BETA.-cells: role of protein palmitoylation in glucose-induced insulin secretion
Author; YAMADA SATOKO (Gunma Univ., Inst. Molecular and Cellular Regulation, JPN) KOJIMA ITARU (Gunma Univ., Inst. Molecular and Cellular Regulation, JPN)
Journal Title;Seikagaku
Journal Code:G0184A
ISSN:0037-1017
VOL.77;NO.6;PAGE.505-510(2005)
Figure&Table&Reference;
Pub. Country;Japan
Language;Japanese
Abstract;Pancreatic .BETA.-cell is a unique cell that responds to nutrients like glucose and secrets insulin. Because insulin secretion is already selectively inhibited by glucose during the process from before the onset to the early stage of diabetes mellitus, understanding the insulin secretion mechanism of normal .BETA.-cell is important for understanding the disease state of the disease and developing new treatments for the disease. This article discusses the insulin secretion mechanism of .BETA.-cell as it is believed at present. It also describes the possibility that long-chain acyl CoA, a lipid metabolism signal formed by glucose stimulation, is involved in the secretion through palmitoylation of protein. In addition, it outlines the result of our study in which an attempt was made to identify a palmitolation target protein that underwent metabolism-dependent palmitoylation changes and discusses the palmitoylated protein and its function in pancreatic .BETA.-cell. (Author's abstract).
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