AMPK and Exercise: Glucose Uptake and Insulin Sensitivity.
- Author:
Hayley M O'NEILL
1
Author Information
- Publication Type:Review
- Keywords: AMPK; Exercise; Glucose uptake; Insulin resistance; Obesity
- MeSH: Animals; Glucose; Glycogen; Insulin; Insulin Resistance; Mice; Organelle Biogenesis; Muscle, Skeletal; Obesity
- From:Diabetes & Metabolism Journal 2013;37(1):1-21
- CountryRepublic of Korea
- Language:English
- Abstract: 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).
