Position title: Associate Professor of Nutritional Sciences
I have long-standing interests in understanding the mechanisms by which intestinal lipid processing modulates systemic metabolism, with a current focus on the metabolic effects of the interplay between diet, host, and gut microbiota. Our research primarily examines the physiological functions of intestinal enzymes involved in the storage and use of fatty acids in health and disease. We discovered that acyl CoA:monoacylglycerol acyltransferase 2 (MGAT2) mediates fat absorption in the intestine and regulates whole body energy expenditure. Mice without a functional MGAT2 gene (Mogat2–/–) exhibit delayed fat absorption and resistance to diet-induced obesity and related metabolic disorders. Surprisingly, we found that Mogat2–/– mice are protected from the pancreatic beta-cell toxin streptozotocin, implicating MGAT2 inhibition as a means to prevent diabetes. We found that both Mogat2–/– mice and intestine-specific MGAT2 knockout mice have increased plasma bile acid levels with altered composition, suggesting a novel circuit between intestinal MGAT2- mediated lipid processing, pancreatic beta-cell function and systemic energy balance.