AMPK regulation of fatty acid metabolism and mitochondrial biogenesis: Implications for obesity

MOLECULAR AND CELLULAR ENDOCRINOLOGY

卷:366

Review

O'Neill, Hayley M.^1,2  Holloway, Graham P.³  Steinberg, Gregory R.² 

[1] Univ Melbourne, Dept Med, St Vincents Inst Med Res, Fitzroy, Vic 3065, Australia

[2] McMaster Univ, Dept Med, Hamilton, ON L8N 3Z5, Canada

[3] Univ Guelph, Dept Human Hlth & Nutr Sci, Guelph, ON N1G 2W1, Canada

关键词: AMPK;    Obesity;    Insulin resistance;    Exercise;    Fatty acid;    Mitochondria;   

DOI  :  10.1016/j.mce.2012.06.019

来源: Elsevier

【 摘 要 】

Skeletal muscle plays an important role in regulating whole-body energy expenditure given it is a major site for glucose and lipid oxidation. Obesity and type 2 diabetes are causally linked through their association with skeletal muscle insulin resistance, while conversely exercise is known to improve whole body glucose homeostasis simultaneously with muscle insulin sensitivity. Exercise activates skeletal muscle AMP-activated protein kinase (AMPK). AMPK plays a role in regulating exercise capacity, skeletal muscle mitochondria] content and contraction-stimulated glucose uptake. Skeletal muscle AMPK is also thought to be important for regulating fatty acid metabolism; however, direct genetic evidence in this area is currently lacking. This review will discuss the current paradigms regarding the influence of AMPK in regulating skeletal muscle fatty acid metabolism and mitochondrial biogenesis at rest and during exercise, and highlight the potential implications in the development of insulin resistance. Crown Copyright (C) 2012 Published by Elsevier Ireland Ltd. All rights reserved.

【 授权许可】

Free