MGAT2 deficiency alters bile acid metabolism

MGAT2 deficient mice (Mogat2—/—) are protected from obesity and hyperglycemia. We hypothesize that altered bile acid (BA) signaling contributes to these protective effects. The present study investigates whether Mogat2—/— mice have altered BA metabolism. BA concentrations were quantified in tissue, fecal and plasma samples from Mogat2—/— and wildtype mice using an enzymatic method. Individual BA species were quantified in plasma via chromatography/mass spectrometry. Expression levels of several BA metabolism and signaling genes were assessed using quantitative PCR. We found that Mogat2—/— mice have elevated plasma BA concentrations, with high proportions of β-muricholic acid and cholic acid species in circulation. These mice also exhibit altered expression of BA signaling and transport genes in the liver and intestine, suggesting that MGAT2 deficiency leads to altered BA signaling. Further investigation of the potential role of BAs in the metabolic phenotype of Mogat2—/— mice is warranted