My research group’s interest lie in the pathogenesis of type 2 diabetes and obesity.  In particular, we are interested in genotype-phenotype relationships and how genetic variation contributes to the pathogenesis of disease.  My group has been involved in the discovery of genetic variation underlying risk for type 2 diabetes and obesity and also contributing to variation in diabetes- and obesity-related traits.  Recently, we have switched our focus to assessing how genetic variants alter biology to contribute to disease.

Our approach is to focus on studies in humans.  This choice is based on a couple of principles.  First, although variants identified by genome-wide association (GWA) may not be “the” functional variant, these variants must be in sufficient linkage disequilibrium with “the” functional variant for us to believe it contributes to disease risk.  Thus, the GWA variant should be more than sufficient to stratify individuals to examine the potential biologic effect of “the” functional variant.  Second, while it may seem prudent to use animal models to examine the underlying biology of genetic variation, in the field of diabetes many times results from animal models have not translated to humans.  Thus, we have chosen to go back to the human model for our studies.  This approach limits some of the things we can do and includes a whole host of unique challenges, but we can at least be assured that our findings are likely to directly add to our knowledge of the pathogenesis of these diseases.  Finally, we are applying a mixture of sophisticated phenotyping and applied mathematics to our studies.  This potent combination allows us to extend our ability to quantify biologic processes we cannot directly measure.