There is a pressing need for new therapeutic strategies to address the epidemic of obesity and its co-morbidities. Bariatric surgery, a surgical manipulation of the gut for weight loss, causes remarkable improvements in obesity and several of its co-morbidities. Specifically, bariatric surgery causes remission of type 2 diabetes (T2DM) and cardiovascular diseases (CVD) such as hypertension. Bariatric surgery also substantially decreases the risk of cancer. Importantly, the metabolic benefits of bariatric surgery often occur prior to weight loss, suggesting that mechanisms other than body weight contribute. Identification of the mechanisms underlying these surgically-induced benefits will provide insight into the basic biology by which the gut regulates whole body physiology, leading to the development of novel therapies for managing obesity and its co-morbidities. Thus, the overall theme of our research program is identifying the mechanisms by which bariatric surgery causes these health benefits using animal models of bariatric surgery. The primary mechanisms of interest in our lab are glucagon-like peptide-1 (GLP-1) and bile acid signaling.
