The direct effect of leptin on skeletal muscle thermogenesis is mediated by substrate cycling between de novo lipogenesis and lipid oxidation

被引：86

作者：

Solinas, G

Summermatter, S

Mainieri, D

Gubler, M

Pirola, L

Wymann, MP

Rusconi, S

Montani, JP

Seydoux, J

Dulloo, AG ^{[1
]}

机构：

[1] Univ Fribourg, Dept Med, Div Physiol, CH-1700 Fribourg, Switzerland

[2] Univ Fribourg, Dept Med, Div Biochem, Fribourg, Switzerland

[3] Fac Med Nice, INSERM, F-06034 Nice, France

[4] Univ Geneva, Fac Med, Dept Physiol, Geneva, Switzerland

来源：

FEBS LETTERS | 2004年 / 577卷 / 03期

关键词：

obesity; diabetes; lipotoxicity; gluco-lipotoxicity; insulin resistance; phosphatidylinositol; 3-kinase; AMP-activated protein kinase; sterol regulatory element; binding protein-lc;

D O I：

10.1016/j.febslet.2004.10.066

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 report here studies that integrate data of respiration rate from mouse skeletal muscle in response to leptin and pharmacological interference with intermediary metabolism, together with assays for phosphatidylinositol 3-kinase (PI3K) and AMP-activated protein kinase (AMPK). Our results suggest that the direct effect of leptin in stimulating thermogenesis in skeletal muscle is mediated by substrate cycling between de novo lipogenesis and lipid oxidation, and that this cycle requires both PI3K and AMPK signaling. This substrate cycling linking glucose and lipid metabolism to thermogenesis provides a novel thermogenic mechanism by which leptin protects skeletal muscle from excessive fat storage and lipotoxicity. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：539 / 544

页数：6

共 20 条

[1] POTASSIUM-INDUCED INCREASE IN OXYGEN-CONSUMPTION OF BROWN ADIPOSE-TISSUE FROM RAT [J].