A Pragmatic Approach Towards the Molecular Mechanisms of Dexamethasone induced Insulin Resistance and Diabetes Mellitus.

Dexamethasone is a glucocorticoid analogue and acts like the hormone cortisol, which is secreted from the adrenal glands. Its prolonged use may alter glucose metabolism. This review is a detailed summary of the underlying molecular mechanism of dexamethasone induced Insulin Resistance and Diabetes Mellitus. A decade of review journals retrieved from Scopus, ScienceDirect, PubMed, and Web of Science databases are systematically analyzed to examine various mechanisms involved in dexamethasone-induced metabolic syndrome. This in vivo model is suitable for studying Diabetes. Impaired insulin sensitivity is a biological response to insulin stimulation in target tissues. This review describes the underlying Dexamethasone-induced Insulin Resistance through multiple molecular mechanisms including decreased expression of glucose transporter protein 1 and 2 (GLUT 1and GLUT 2), glycogen synthase, increased expression of FK506 binding protein 5 (FKBP5), Cx36 protein, GSK-3, altered metabolism, and GLUT 4 transporter expression, mitochondrial dysfunction, defective glucose uptake, inflammation, insulin receptor mutations, stimulation of protein kinase C, oxygen species induced stress, protein folding stress, endothelial dysfunction, suppression of phosphatidylinositol 3 kinase (P13K) activity associated with IRS-1. Significant metabolic alterations triggered by dexamethasone treatment interposed with typical blood sugar homeostasis. Future research should concentrate on methods to avoid insulin resistance caused by dexamethasone without compromising the pharmacotherapeutic effect. Living with insulin resistance in the long run can lead to type 2 diabetes along with other complications. In discriminate use of Dexamethasone is the culprit behind the development of abnormal insulin action. Overall, a better insight in this regard is the need of the hour. Furthermore, work is essential towards the development of new molecules to provide a better substitute in the Reck.