期刊
FEBS LETTERS
卷 577, 期 3, 页码 539-544出版社
WILEY
DOI: 10.1016/j.febslet.2004.10.066
关键词
obesity; diabetes; lipotoxicity; gluco-lipotoxicity; insulin resistance; phosphatidylinositol 3-kinase; AMP-activated protein kinase; sterol regulatory element; binding protein-lc
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.
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