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Turning Foes to Friends: Knocking Down Diabetes Associated SGLT2 Transporters and Sustaining Life

Authors :
Gupta, Ankit
Mittal, Sheenu
Monika
Dhingra, Richa
Dhingra, Neelima
Source :
Current Diabetes Reviews; September 2020, Vol. 16 Issue: 7 p716-732, 17p
Publication Year :
2020

Abstract

Background: The discovery of Sodium-Glucose co-transporter-2 (SGLT2) inhibitors had rewritten the treatment of diabetes mellitus with an impressive fall in the incidence of death and associated complications. Introduction: The SGLT2 inhibitors by inhibiting the SGLT2 in the proximal nephron, helps in reducing the reabsorption of approximately 90% of the filtered glucose and increased urinary glucose excretion (UGE). Methods: The literature related to SGLT2 inhibitors has been thoroughly explored from various available public domains and reviewed extensively for this article. Detailed and updated information related to SGLT2 inhibitors with a major focus on the recently approved Ertuglifolzin is structured in this review. Result: The present review is an effort to understand the management of diabetes mellitus over the past few decades with a special focus on the role of SGLT2 receptor in the causes of therapeutic and preventive strategies for diabetes mellitus. Pragmatic placement of the currently available Canagliflozin, Dapagliflozin, and Empagliflozin as oral antidiabetic agents has been done. Well accommodated stereochemistry and a high docking score of Ertugliflozin in ligand-receptor simulation studies attribute to its high potency. Conclusion: This review highlights the unique mechanism of SGLT2 Inhibitors coupled with pleiotropic benefits on weight and blood pressure, which make it an attractive choice of therapy to diabetic patients, not controlled by other medications.

Details

Language :
English
ISSN :
15733998
Volume :
16
Issue :
7
Database :
Supplemental Index
Journal :
Current Diabetes Reviews
Publication Type :
Periodical
Accession number :
ejs53918771
Full Text :
https://doi.org/10.2174/1573399816666200117155016