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Role of Glycogen Synthase Kinase-3 in the Etiology of Type 2 Diabetes Mellitus: A Review.

Abstract
The risk of type 2 diabetes mellitus (T2DM) is increasing abundantly due to lifestyle-related obesity and associated cardiovascular problems. Presently, Glycogen synthase kinase-3 (GSK-3) has gained considerable attention from biomedical scientists to treat diabetes. Phosphorylation of GSK-3 permits a number of cellular activities like regulation of cell signaling, cellular metabolism, cell proliferation and cellular transport. Inhibiting GSK-3 activity by pharmacological intervention has become an important strategy for the management of T2DM. This review focuses on the schematic representation of fundamental GSK-3 enzymology and encompasses the GSK-3 inhibitors as a future therapeutic lead target for the management of T2DM that may significantly regulate insulin sensitivity to insulin receptor, glycogen synthesis and glucose metabolism. The various signaling mechanisms of inhibiting the GSK-3 by describing insulin signaling through Insulin Receptor Substrate (IRS-1), Phosphatidylinositol-3 Kinase (PI3K) and Protein Kinase B (PKB/ AKT) pathways that may hopefully facilitate the pharmacologist to design for antidiabetic drug evaluation model in near future have also been highlighted.
AuthorsAsis Bala, Susmita Roy, Debanjana Das, Venkatesh Marturi, Chaitali Mondal, Susmita Patra, Pallab Kanti Haldar, Gourav Samajdar
JournalCurrent diabetes reviews (Curr Diabetes Rev) Vol. 18 Issue 3 Pg. e300721195147 ( 2022) ISSN: 1875-6417 [Electronic] United Arab Emirates
PMID34376135 (Publication Type: Journal Article, Review)
CopyrightCopyright© Bentham Science Publishers; For any queries, please email at [email protected].
Chemical References
  • Insulin
  • Receptor, Insulin
  • Glycogen Synthase Kinase 3
Topics
  • Diabetes Mellitus, Type 2 (drug therapy, etiology, metabolism)
  • Glycogen Synthase Kinase 3
  • Humans
  • Insulin (metabolism)
  • Insulin Resistance (physiology)
  • Receptor, Insulin (metabolism)

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