Intracellular Fatty Acid Metabolism in Skeletal Muscle and Insulin Resistance

Title: Intracellular Fatty Acid Metabolism in Skeletal Muscle and Insulin Resistance

Volume: 1 Issue: 3

Author(s): Eun H. Koh, Woo J. Lee, Min-Seon Kim, Joong-Yeol Park, In K. Lee and Ki-Up Lee

Affiliation:

Keywords: triglyceride, fatty acid oxidation, mitochondria, insulin resistance, skeletal muscle, ampk

Abstract: Triglyceride accumulation in skeletal muscle is increased in subjects with insulin resistance. Increased intracellular lipolysis from stored triglyceride may induce insulin resistance in skeletal muscle by activating the glucosefatty acid cycle. However, inconsistent with this hypothesis, intracellular lipolysis from skeletal muscle is decreased in high fat-fed, insulin resistant rats. Therefore, it is suggested that an increase in triglyceride accumulation is the result of decreased mitochondrial fatty acid oxidation in the cells. As evidence, fenofibrate (a PPARα activator), rosiglitazone (a PPARγ activator) and alpha-lipoic acid completely prevented the development of diabetes in obese diabetes-prone rats. All three drugs increased fatty acid oxidation and decreased triglyceride accumulation in skeletal muscle. Administration of ALA activated AMPK and increased fatty acid oxidation. It is suggested that decreased fatty acid oxidation in skeletal muscle is one of the major factors leading to an accumulation of lipid metabolites and insulin resistance.

Cite this article as:

Koh H. Eun, Lee J. Woo, Kim Min-Seon, Park Joong-Yeol, Lee K. In and Lee Ki-Up, Intracellular Fatty Acid Metabolism in Skeletal Muscle and Insulin Resistance, Current Diabetes Reviews 2005; 1 (3) . https://dx.doi.org/10.2174/157339905774574347