Regulation of Type-2 Diabetes through IP3R and MTrs along with SERCA and CRAC Channels by Agomelatine, Luzindol, 2-APB and Thapsigargin: A Computational Exploration

Abstract

Type-2 diabetes speedily disseminates from corner to corner in the humanity. Activation of insulin secretion mainly depends on melatonin receptors, IP3 receptor as well as sarcoplasmic endoplasmic reticulum Ca2+ ATPase channel. Agomelatine and IP3 have a very important role in the increased Ca2+ level in the cytoplasm followed by the secretion of insulin; both are the activator of MTrs and IP3 receptors respectively. Luzindol and 2-APB are the inhibitor of MTrs and IP3 receptor, mediated by the inhibition of the PLC pathway caused reduction of IP3 which is a very important element for the insulin secretion. Keyhitch in type-2 diabetes is failing the quantity of insulin in the pancreas by exhaustion of Ca2+ in cytoplasm. IP3 will be activated by the existence of agomelatine consequential in elevation of the Ca2+ level in the cytoplasm follow by lack of Ca2+ levels in the endoplasmic reticulum. Collectively, our computational studies suggest that MTrs and IP3 R are the narrative and hopeful targets to be used against type-2 diabetes.