IA-2β, but not IA-2, is induced by ghrelin and inhibits glucose-stimulated insulin secretion

被引：56

作者：

Doi, A ^{[1
]}

Shono, T ^{[1
]}

Nishi, M ^{[1
]}

Furuta, H ^{[1
]}

Sasaki, H ^{[1
]}

Nanjo, K ^{[1
]}

机构：

[1] Wakayama Med Univ, Dept Med 1, Wakayama 6418509, Japan

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2006年 / 103卷 / 04期

关键词：

protein tyrosine phosphatase; secretary granule;

D O I：

10.1073/pnas.0502470102

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Ghrelin is a newly discovered peptide and an endogenous ligand for growth hormone (GH) secretagogue (GHS) receptor. It has been shown to possess various central and peripheral effects, including GH secretion, food intake, and gastric and cardiac effects. Ghrelin and the GHS receptor are expressed also in pancreatic islets. We have identified several ghrelin-induced genes by PCR-select subtraction methods, among which is a p-cell autoantigen for type 1 diabetes, IA-2 beta. Administration of ghrelin increased IA-2 beta mRNA in mouse brain, pancreas, and insulinoma cell lines (MINIS and beta TC3). However, the expression of IA-2, another structurally related beta-cell autoantigen, was not induced by ghrelin. Administration of ghrelin or overexpression of IA-2 beta, but not overexpression of IA-2, inhibited glucose-stimulated insulin secretion in MIN6 insulinoma cells and, moreover, inhibition of IA-2 beta expression by the RNA interference technique ameliorated ghrelin's inhibitory effects on glucose-stimulated insulin secretion. These findings strongly suggest that inhibitory effects of ghrelin on glucose-stimulated insulin secretion are at least partly due to increased expression of IA-2 beta induced by ghrelin. Our data demonstrate the link among ghrelin, IA-2 beta, and glucose-stimulated insulin secretion.

引用

页码：885 / 890

页数：6

共 38 条

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