Dr. Craig Stump has made important contributions in the areas of skeletal muscle biology and the role of exercise and lifestyle in the etiology of insulin signaling abnormalities, and the development of the metabolic syndrome and diabetes. He has seminal papers that contribute to our understanding of the role of skeletal muscle mitochondrial function in health and disease. He also investigates the link between the renin-angiotension system and tissue resistance to insulin, and identifying biomarkers related to the risk of developing diabetes and diabetic complications.
Dr. Stump collaborates with other University of Arizona investigators regarding co-morbidities related to cardiovascular and kidney disease as well as to implement the Diabetes Prevention Program into specific high-risk populations, and with an Arizona State University team dedicated to developing and bringing to clinical utility personal devices designed to monitor and improve metabolic health. He is also a site principal investigator for several pharmaceutical trials testing new medications for diabetic patients. He is, in conjunction with the Arizona Proteomics Consortium, working to identify modified protein biomarker(s) of diabetes and pre-diabetes which would lead to early diagnosis and treatment.
Research activities include:
- Determining the effect of angiotensin II on skeletal muscle NAD(P)H oxidase activity and reactive oxygen species using Ren-2 transgenic and Zucker obese rat models, and myoblast/myotube cell cultures.
- Determining the effects of angiotensin II receptor or mineralcorticoid receptor blockade on skeletal muscle insulin signaling and glucose transport.
- Determining the effects of physical inactivity, mitochondrial dysfunction, and ectopic lipid accumulation on NAD(P)H oxidase activity, oxidative stress and tissue resistance to insulin.
- Determining the role of inflammatory cytokines on the development of tissue insulin resistance in skeletal muscle cell cultures, and hypertensive and obese animal models.
- Determining the mechanisms by which insulin up-regulates skeletal muscle mitochondrial oxidative capacity.