Research Projects

CD36 (Cluster of differentiation 36) is a multi-ligand membrane glycoprotein receptor contributing to glucose and lipid metabolism. CD36 has been found to be expressed in cells associated with metabolic abnormalities related to prediabetes and diabetes mellitus. Its function relates to the modulation of the inflammatory response caused by oxidative stress resultant alterations in major metabolic pathways. Moreover, soluble CD36 (sCD36) level was found to increase consistently with abnormal glucose tolerance and associated with risk of Diabetes Mellitus (DM). Further, studies suggested that CD36 is closely related to β-cell dysfunction and insulin resistance but the physiological mechanism is not yet known. The effect of genetic variants in CD36 also suggested its strong association in determining the Type 2 Diabetes Mellitus (T2DM) susceptibility among the North Indian population. Thus, CD36 is a major “candidate” protein associated with the pathogenesis of DM. It is hypothesized in the proposed work that CD36activates PPARγ and NFĸB via PKC signaling and influence their regulation. This leads to activation of P38MAPK, JNK/SAPK and JAK/STAT signaling pathways resulting in β-cell and insulin dysfunction. In the present study, the focus will be to explore the effect of CD36 inactivation on the expression of upstream and downstream signaling molecules. The CD36 in pancreatic β cells will be inactivated by the inhibitor Sulfo-N-SuccinimidylOleate (SSO). The proteins and RNA from CD36+, CD36- and HEK cells as control will be subjected to proteomic and transcriptomic analyses in order to identify the CD36 target molecules which can be utilized in therapeutics of DM. The expected outcome and significance of the proposal is to establish the physiological role/action of CD36 and mediated signaling during DM.CD36 targeted molecules may be further subjected to the development of therapeutic agents and prognostic markers for DM.