L-arginine prevents metabolic effects of high glucose in diabetic mice

被引：22

作者：

West, Matthew B. ^{[2
]}

Ramana, Kota V. ^{[3
]}

Kaiserova, Karin ^{[2
]}

Srivastava, Satish K. ^{[3
]}

Bhatnagar, Aruni ^{[1
,2
]}

机构：

[1] Univ Louisville, Div Cardiol, Dept Med, Inst Mol Cardiol, Louisville, KY 40202 USA

[2] Univ Louisville, Dept Biochem & Mol Biol, Louisville, KY 40202 USA

[3] Univ Texas Galveston, Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA

来源：

FEBS LETTERS | 2008年 / 582卷 / 17期

关键词：

nitric oxide; diabetes mellitus; cell adhesion molecule; signal transduction; inflammation;

D O I：

10.1016/j.febslet.2008.06.039

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We tested the hypothesis that activation of the polyol pathway and protein kinase C ( PKC) during diabetes is due to loss of NO. Our results show that after 4 weeks of streptozotocininduced diabetes, treatment with L- arginine restored NO levels and prevented tissue accumulation of sorbitol in mice, which was accompanied by an increase in glutathiolation of aldose reductase. L- Arginine treatment decreased superoxide generation in the aorta, total PKC activity and PKC- bII phosphorylation in the heart, and the plasma levels of triglycerides and soluble ICAM. These data suggest that increasing NO bioavailability by L- arginine corrects the major biochemical abnormalities of diabetes. (c) 2008 Published by Elsevier B. V. on behalf of the Federation of European Biochemical Societies.

引用

页码：2609 / 2614

页数：6

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