Regulation of exercise-stimulated glucose uptake in skeletal muscle.
10.6065/apem.2016.21.2.61
- Author:
Ho Jin KOH
1
Author Information
1. Applied Physiology Division, Department of Exercise Science, Arnold School of Public Health, Univer sity of South Carolina, Columbia, SC, USA. kohh@mailbox.sc.edu
- Publication Type:Review
- Keywords:
Skeletal muscle;
Glucose uptake;
Exercise;
Obesity;
Insulin
- MeSH:
AMP-Activated Protein Kinases;
Animals;
Glucose*;
Insulin;
Insulin Resistance;
Liver;
Mice;
Mice, Knockout;
Muscle, Skeletal*;
Obesity;
Phosphotransferases;
Protein Kinases
- From:Annals of Pediatric Endocrinology & Metabolism
2016;21(2):61-65
- CountryRepublic of Korea
- Language:English
-
Abstract:
AMP-activated protein kinase (AMPK) is a Ser/Thr kinase that has been thought to be an important mediator for exercise-stimulated glucose uptake in skeletal muscle. Liver kinase B1 (LKB1) is an upstream kinase for AMPK and AMPK-related protein kinases, of which the function in skeletal muscle has not been well documented. Our group and others have generated mice lacking AMPK activity in skeletal muscle, as well as muscle-specific LKB1 knockout mice. In this review, we discuss the potential role of AMPK and LKB1 in regulating exercise-stimulated glucose uptake in skeletal muscle. We also discuss our recent study, demonstrating the molecular mechanism of obesity-induced development of skeletal muscle insulin resistance.
