MCT Blocks Lipogenesis Through Ppar Gamma

I've been using coconut oil to get an adequate intake of saturated fats when my red meat intake is low. I've noticed an increase in energy and better skin as the most outstanding benefits.

Here's another cool benefit I've stumbled upon.

"Nutr Metab (Lond). 2006 Jul 27;3(1):30 [Epub ahead of print] Related Articles, Links


Modulation of adipocyte lipogenesis by octanoate: involvement of reactive oxygen species.

Guo W, Xie W, Han J.

ABSTRACT: BACKGROUND: Octanoate is a medium-chain fatty acid (MCFA) that is rich in milk, coconut oil and other tropical dietary lipids. Octanoate accounts for about 70% of the fatty acids in commercial MCT oil. Use of dietary MCT for weight control can be tracked to early 1950s, and is highlighted by several recent clinical trials. The molecular mechanisms of the weight reduction effect remain not completely understood. Prior studies considered the rapid hepatic oxidation of MCFA as the main cause for a deficiency in fatty acid supply to the peripheral tissues. However, we and others found that significant amounts of MCFA are recovered in adipose tissue in MCT-fed animals and humans, implying that there might be 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 (PPARgamma) and its associated lipogenic genes were assessed. In selected experiments, long-chain fatty acid oleate, PPARgamma agonist troglitazone, and antioxidant N-acetylcysteine were used in parallel. Effects of insulin, L-carnitine, and etomoxir on beta-oxidation of octanoate and oleate were measured as possible mechanism for increased ROS production. Results: beta-oxidation was inhibited by insulin moderately (18%) for octanoate as compared with oleate (60%). Under conditions that normally favor lipogenesis in adipocytes (170 nM insulin (170 nM) and 25 mM glucose), octanoate inhibited triglyceride synthesis, reduced expression of lipogenic genes and inhibited PPARgamma transcription activity, in association with increased ROS. Co-treatment with troglitazone, N-acetylcysteine, or over-expression of glutathione peroxidase 1 blocks the anti-lipogenic effects of octanoate. Conclusion: these findings support our hypothesis that MCFA-induced fat mass loss can be at least partially explained by the octanoate-mediated inactivation of PPARgamma, which leads to a pleiotropic down regulation of anabolic genes and inhibition on lipogenesis in adipocytes. Furthermore, our data suggest that ROS might play an important role in this process.

PMID: 16872526"