Modulation of Adipocyte Lipogenesis by Octanoate: Involvement of Reactive Oxygen Species
Date
2006-7-27
Authors
Guo, Wen
Xie, Weisheng
Han, Jianrong
Version
OA Version
Citation
Guo, Wen, Weisheng Xie, Jianrong Han. "Modulation of adipocyte lipogenesis by octanoate: involvement of reactive oxygen species" Nutrition & Metabolism 3:30. (2006)
Abstract
BACKGROUND. Octanoate is a medium-chain fatty acid (MCFA) that is rich in milk and tropical dietary lipids. It also accounts for 70% of the fatty acids in commercial medium chain triglycerides (MCT). Use of MCT for weight control tracks back to early 1950s and is highlighted by recent clinical trials. The molecular mechanisms of the weight reduction effect remain not completely understood. The findings of significant amounts of MCFA in adipose tissue in MCT-fed animals and humans suggest a direct influence of MCFA on fat cell functions. METHODS. 3T3-L1 adipocytes were treated with octanoate in a high glucose culture medium supplemented with 10% fetal bovine serum and 170 nM insulin. The effects on lipogenesis, fatty acid oxidation, cellular concentration of reactive oxygen species (ROS), and the expression and activity of peroxisome proliferator receptor gamma (PPARγ) and its associated lipogenic genes were assessed. In selected experiments, long-chain fatty acid oleate, PPARγ agonist troglitazone, and antioxidant N-acetylcysteine were used in parallel. Effects of insulin, L-carnitine, and etomoxir on β-oxidation were also measured. RESULTS. β-oxidation of octanoate was primarily independent of CPT-I. Treatment with octanoate was linked to an increase in ROS in adipocytes, a decrease in triglyceride synthesis, and reduction of lipogenic gene expression. Co-treatment with troglitazone, N-acetylcysteine, or over-expression of glutathione peroxidase largely reversed the effects of octanoate. CONCLUSION. These findings suggest that octanoate-mediated inactivation of PPARγ might contribute to the down regulation of lipogenic genes in adipocytes, and ROS appears to be involved as a mediator in this process.
Description
License
Copyright 2006 Guo et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.