Co-Associate Director and Scientific Council member, Jane E. B. Reusch, M.D. is a Professor of Medicine and Biochemistry at the University of Colorado Denver and Denver VAMC. She graduated from the University of Notre Dame and attended medical school at Northwestern University and the University of Minnesota. Dr. Reusch did her internal medicine, endocrinology, diabetes, and metabolism training at the University of Colorado Health Sciences Center. Dr. Reusch is Past-President of the American Federation for Medical Research Foundation, and she is a member of the American Diabetes Association, the American Society for Clinical Investigation, the American Association of Physicians, the American Heart Association, the Juvenile Diabetes Research Foundation, The Endocrine Society, and the American Heart Association. Dr. Reusch is currently on the FASEB Board Science Policy Committee where she represents the interests of clinical research and the need to have a workforce of clinical investigators to translate scientific advances to patients in the community.
Dr Reusch leads a translational research program which
seeks to understand the molecular barriers to optimal exercise function in
adults and children with Type 1 and Type 2 Diabetes Mellitus. In her
collaborative research program with Dr Regensteiner, they have characterized
defects in maximal and submaximal exercise capacity. In human subjects,
this dysfunction correlates with insulin resistance, endothelial dysfunction,
decreased perfusion of the heart and skeletal muscle and decreased
mitochondrial function. Treatment with the insulin
sensitizer rosiglitazone augments functional exercise capacity in
sedentary people with type 2 diabetes. This serves as proof of concept that
targeting the functional defects can improve the exercise dysfunction.
The Reusch lab
was recently awarded a VA merit award to investigate the heart and vascular
response to exercise training in rodent models of type 2 diabetes. She
made the novel and disconcerting observation that mitochondrial adaptive
changes induced by exercise are blunted in diabetic rodent models. They
have identified that nitric oxide synthase dysfunction contributes to
failed adaptation and have exciting preliminary results suggesting that a
new class of diabetes drugs can restore endothelial nitric oxide synthase
function and augment the beneficial response to exercise training and diabetes.
This finding will support a 4 year investigation of molecular barriers to
exercise is diabetes. Ongoing studies with Dr. Regensteiner are evaluating
these same interventions in human subjects with diabetes.