ISSN: 2155-9880
+44 1300 500008
Hema Viswambharan
University of Leeds, UK
Posters & Accepted Abstracts: J Clin Exp Cardiolog
Insulin resistance at a whole body level and in the endothelium is shown to be a hallmark of Type 2 diabetes. Insulin resistance in the endothelium reduces bioavailability of nitric oxide (NO), which is well established for its anti-atherosclerotic effects on the vasculature. The molecular effects of perturbations in insulin sensitivity particularly in the endothelium have not been widely investigated. We studied different models of insulin sensitivity and its effects in mediating atherosclerosis and cardiovascular complications. Different experimental models of insulin resistance at a whole-body level and specific to the endothelium demonstrated that insulin resistance eventually leads to an increase in generation of reactive oxygen species and accelerated atherosclerosis via the insulin receptor signaling pathways. These mice have also demonstrated impaired acetylcholine-induced aortic relaxation. This impairment could be reversed by NADPH oxidase inhibitors suggesting a role of reactive oxygen species in mediating insulin resistance and endothelial dysfunction.
Email: H.Viswambharan@leeds.ac.uk