Improved glucose control and reduced body fat mass in free fatty acid receptor2-deficient mice fed a high-fat diet.

摘要

Free fatty acid receptor 2 (Ffar2), also known as GPR43, is activated byshort-chain fatty acids (SCFA) and expressed in intestine, adipocytes, and immunecells, suggesting involvement in lipid and immune regulation. In the presentstudy, Ffar2-deficient mice (Ffar2-KO) were given a high-fat diet (HFD) or chowdiet and studied with respect to lipid and energy metabolism. On a HFD, Ffar2-KO mice had lower body fat mass and increased lean body mass. The changed bodycomposition was accompanied by improved glucose control and lower HOMA index,indicating improved insulin sensitivity in Ffar2-KO mice. Moreover, the Ffar2-KO mice had higher energy expenditure accompanied by higher core body temperatureand increased food intake. The liver weight and content of triglycerides as well as plasma levels of cholesterol were lower in the Ffar2-KO mice fed a HFD. Ahistological examination unveiled decreased lipid interspersed in brown adiposetissue of the Ffar2-KO mice. Interestingly, no significant differences in whiteadipose tissue (WAT) cell size were observed, but significantly lower macrophage content was detected in WAT from HFD-fed Ffar2-KO compared with wild-type mice.In conclusion, Ffar2 deficiency protects from HFD-induced obesity anddyslipidemia at least partly via increased energy expenditure.