Dr. Kirk M. Habegger is Assistant Professor of Medicine in the Division of Endocrinology, Diabetes, and Metabolism. He obtained his Ph.D. in Biochemistry and Molecular Biology from Indiana University School of Medicine in 2006. He conducted his postdoctoral training under the mentorship of Drs. Matthias Tschoep and Randy Seeley at the Metabolic Diseases Institute of the University of Cincinnati from 2009 to 2013. He was promoted to the faculty at UC in the Department of Medicine, before leaving to start his group at UAB.
Dr. Habegger is the recipient of the American Diabetes Assoc. Junior Faculty Career Development award as well as a K01 Career Development award through the NIDDK-NIH. His research is targeted on a search for the molecular underpinnings of the onset and progression of Diabetes and Obesity, as well as the development of potential treatments. His work aims to discover and dissect neuroendocrine and peripheral signaling pathways that regulate energy, glucose and lipid metabolism. Many of the projects in the Habegger group investigate novel pharmacological therapies against diabetes and obesity in rodent models. Current projects include 1) the non-cannonical aspects of glucagon biology including its role in the adaptive response to exercise and 2) CNS integration of nutrient sensing.
Abstract
Several bariatric operations are currently used to treat obesity and obesity-related comorbidities. These vary in efficacy, but most are more effective than current pharmaceutical treatments. Roux-en-Y gastric bypass (RYGB) produces substantial body weight (BW) loss and enhanced glucose tolerance, and is associated with increased secretion of the gut hormone glucagon-like peptide 1 (GLP-1). Given the success of GLP-1–based agents in lowering blood glucose levels and BW, we hypothesized that an individual sensitivity to GLP-1 receptor agonism could predict metabolic benefits of surgeries associated with increased GLP-1 secretion. One hundred ninety-seven high-fat diet–induced obese male Long-Evans rats were monitored for BW loss during exendin-4 (Ex4) administration. Stable populations of responders and nonresponders were identified based on Ex4-induced BW loss and GLP-1–induced improvements in glucose tolerance. Subpopulations of Ex4 extreme responders and nonresponders underwent RYGB surgery. After RYGB, responders and nonresponders showed similar BW loss compared with sham, but nonresponders retained impaired glucose tolerance. These data indicate that the GLP-1 response tests may predict some but not all of the improvements observed after RYGB. These findings present an opportunity to optimize the use of bariatric surgery based on an improved understanding of GLP-1 biology and suggest an opportunity for a more personalized therapeutic approach to the metabolic syndrome.
