Glucose-induced production of hydrogen sulfide may protect the pancreatic beta-cells from apoptotic cell death by high glucose

被引：78

作者：

Kaneko, Yukiko ^{[1
,2
]}

Kimura, Toshihide ^{[1
]}

Taniguchi, Shigeki ^{[1
]}

Souma, Midori ^{[1
]}

Kojima, Yumiko ^{[2
]}

Kimura, Yuka ^{[3
]}

Kimura, Hideo ^{[3
]}

Niki, Ichiro ^{[1
]}

机构：

[1] Oita Univ, Fac Med, Dept Pharmacol, Oita 8795593, Japan

[2] Univ Shizuoka, Sch Pharmaceut Sci, Dept Pharmacol, Suruga Ku, Shizuoka 4228526, Japan

[3] Natl Inst Neurosci, Dept Mol Genet, Tokyo 1878551, Japan

来源：

FEBS LETTERS | 2009年 / 583卷 / 02期

关键词：

Hydrogen sulfide; Pancreatic beta-cell; Cystathionine-gamma-lyase (CSE); Cystathionine-beta-synthase (CBS); Apoptosis; L-Cysteine; METABOLISM; DAMAGE; MEDIATOR; MAMMALS; STRESS; RAT;

D O I：

10.1016/j.febslet.2008.12.026

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

We examined the expression of the major H2S-producing enzymes, cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE). CBS was ubiquitously distributed in the mouse pancreas, but CSE was found only in the exocrine. Freshly isolated islets expressed CBS, while CSE was faint. However, high glucose increased the CSE expression in the beta-cells. L-Cysteine or NaHS suppressed islet cell apoptosis with high glucose, and increased glutathione content in MIN6 beta-cells. Pretreatment with L-cysteine improved the secretory responsiveness following stimulation with glucose. The CSE inhibitor DL-propargylglycine antagonized these L-cysteine effects. We suggest H2S may function as an 'intrinsic brake' which protects beta-cells from glucotoxicity. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：377 / 382

页数：6

共 17 条

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INTERORGAN METABOLISM OF AMINO-ACIDS IN STREPTOZOTOCIN-DIABETIC KETOACIDOTIC RAT [J].