Lipid metabolic intermediates regulate skeletal muscle insulin sensitivity.
- Author:
Dan-Dan BAI
1
;
Wei-Hua XIAO
2
Author Information
1. Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai 200438, China.
2. Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai 200438, China. xiaoweihua@sus.edu.cn.
- Publication Type:Journal Article
- MeSH:
Humans;
Insulin Resistance/physiology*;
Muscle, Skeletal/metabolism*;
Insulin/metabolism*;
Lipid Metabolism;
Fatty Acids/metabolism*
- From:
Acta Physiologica Sinica
2022;74(5):805-815
- CountryChina
- Language:Chinese
-
Abstract:
Skeletal muscle is the largest organ of human body, which completes 80%-90% of glucose intake stimulated by insulin, and is closely related to the occurrence and development of insulin resistance (IR). Skeletal muscle is one of the main places of lipid metabolism, and lipid metabolites participate in skeletal muscle metabolism as signal molecules. Fatty acids regulate skeletal muscle insulin sensitivity through insulin signaling pathway, inflammatory response and mitochondrial function. Saturated fatty acids (SFAs) induce insulin resistance by impairing insulin signal transduction, inducing mitochondrial dysfunction and inflammatory response, while unsaturated fatty acids reverse the adverse effects of SFAs and ameliorate IR by enhancing insulin signal transduction and anti-inflammatory effect. In addition, disorders of lipid metabolism in skeletal muscle cause accumulation of harmful metabolic intermediates, such as diacylglycerol, ceramide and long-chain acyl-coenzyme A, and induce IR by directly or indirectly damaging insulin signaling pathway. This article reviews the research progress of lipid metabolic intermediates regulating insulin sensitivity in skeletal muscle, which will help to better understand the pathogenesis of diabetes.
