AMPK and Exercise: Glucose Uptake and Insulin Sensitivity

被引:123
作者
O'Neill, Hayley M. [1 ]
机构
[1] St Vincents Inst Med Res, Prot Chem & Metab Unit, 9 Princes St, Fitzroy, Vic, Australia
关键词
AMPK; Exercise; Glucose uptake; Insulin resistance; Obesity;
D O I
10.4093/dmj.2013.37.1.1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
AMPK is an evolutionary conserved sensor of cellular energy status that is activated during exercise. Pharmacological activation of AMPK promotes glucose uptake, fatty acid oxidation, mitochondrial biogenesis, and insulin sensitivity; processes that are reduced in obesity and contribute to the development of insulin resistance. AMPK deficient mouse models have been used to provide direct genetic evidence either supporting or refuting a role for AMPK in regulating these processes. Exercise promotes glucose uptake by an insulin dependent mechanism involving AMPK. Exercise is important for improving insulin sensitivity; however, it is not known if AMPK is required for these improvements. Understanding how these metabolic processes are regulated is important for the development of new strategies that target obesity-induced insulin resistance. This review will discuss the involvement of AMPK in regulating skeletal muscle metabolism (glucose uptake, glycogen synthesis, and insulin sensitivity).
引用
收藏
页码:1 / 21
页数:21
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