Molecular Mechanism of Insulin Resistance and Type 2 Diabetes

Abstract

Aim: To analyze the relationship between the molecular mechanism of insulin resistance and its associated type-2 diabetes.

Method: Relevant articles were identified via PUBMED, GOOGLE SCHOLAR MeSH, Cochrane, bioRxiv, Semantic scholar search engines using the keywords Insulin receptor, Insulin resistance, signaling, Insulin receptor substrate proteins, Type 2 diabetes mellitus. Period of duration considered was from 1980 to till date.

Discussion: Insulin resistance is a major risk factor for developing type 2 diabetes caused by insulin-target tissue's inability to respond properly to insulin and contributes to obesity morbidity. Insulin action involves a series of signaling cascades initiated by insulin binding to its receptor, causing autophosphorylation of the receptor and activation of the tyrosine kinase receptor, resulting in tyrosine phosphorylation of the insulin receptor substrates (IRSs). Phosphorylation of IRSs contributes to phosphatidylinositol 3-kinase (PI3K) activation and subsequent activation of Akt and its downstream mediator AS160, both of which are critical measures to promote insulin-induced glucose transport.

Conclusion: Identifying signals and understanding the complex relationship of the various factors that modulate insulin sensitivity are important prerequisites for developing new and more specific antidiabetic compounds.. By elucidating the cellular and molecular mechanisms responsible for insulin resistance, these studies provide potential new targets to treat and prevent type 2 diabetes mellitus. This review focuses on the molecular basis of insulin resistance to skeletal muscles and type 2 diabetes.