%0 Journal Article
%T MGAT2 deficiency ameliorates high-fat diet-induced obesity and insulin resistance by inhibiting intestinal fat absorption in mice
%A Takuma Tsuchida
%A Sayaka Fukuda
%A Hisanori Aoyama
%A Nobuhiko Taniuchi
%A Tomomi Ishihara
%A Noriko ohashi
%A Hiroko Sato
%A Koji Wakimoto
%A Masaharu Shiotani
%A Akira Oku
%J Lipids in Health and Disease
%D 2012
%I BioMed Central
%R 10.1186/1476-511x-11-75
%X In oral fat tolerance test (OFTT), Mgat2-deficient mice absorbed less fat into the circulation. When maintained on a high-fat diet (HFD), Mgat2-deficient mice were protected from HFD-induced obesity and insulin resistance. Heterozygote (Mgat2+/£¿) mice had an intermediate phenotype between Mgat2+/+ and Mgat2£¿/£¿ and were partially protected from metabolic disorders. Despite of a decrease in fat absorption in the Mgat2-deficient mice, lipid levels in the feces and small intestine were comparable among the genotypes. Oxygen consumption was increased in the Mgat2-deficient mice when maintained on an HFD. A prominent upregulation of the genes involved in fatty acid oxidation was observed in the duodenum but not in the liver of the Mgat2-deficient mice.These results suggest that MGAT2 has a pivotal role in lipid metabolism in the small intestine, and the inhibition of MGAT2 activity may be a promising strategy for the treatment of obesity-related metabolic disorders.
%K Acyl-coenzyme A:monoacylglycerol acyltransferase (MGAT)
%K Obesity
%K Insulin resistance
%K Triglyceride
%K Enterocyte
%K Fatty acid oxidation
%U http://www.lipidworld.com/content/11/1/75/abstract