Abstract 166: Omega3-Rich Diet Modulates Leptin through Lipid Sensing G-Protein Coupled Receptors in Catalase Transgenic Mice
Diet induced obesity is a major risk factor for cardiometabolic diseases. Oxidative stress plays an important etiological role in these diseases. Hence, we hypothesized that increased antioxidant expression will prevent obesogenic events. We tested our hypothesis by feeding normal chow (nc), high fat diet (HF) and omega-3 rich diet (OM3) to C57Bl/6J mice or human catalase transgenic mice-[Tg(CAT)+/0] (antioxidant enzyme that detoxifies hydrogen peroxide) (n=8) for 6 weeks. Our results indicated no difference in food consumption among the groups, but a significant increase in both body weight and adipose weight on HF fed diet, but not with OM3 diet in Tg(CAT)+/0 mice compared to C57Bl/6J mice. There was a 140-fold induction in leptin mRNA expression in the adipose tissue even at basal levels in Tg(CAT)+/0 mice compared to C57Bl/6J, which was further increased to 170-fold after HF diet. The diet rich in OM3 brought the leptin levels down by <80%. The fluctuations in leptin levels in Tg(CAT)+/0 mice seems to be regulated by changes in lipid sensing PPARγ and G-protein coupled receptors (GPR120, GPR41/43). Our results suggest that increase in antioxidant enzyme catalase modulates leptin pathway. This modulation can be regulated by omega-3 rich diet. The physiological significance of these findings in relation to obesity will be the focus of our future studies.
- © 2013 by American Heart Association, Inc.