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Molecular mechanisms by which SGLT2 inhibitors can induce insulin sensitivity in diabetic milieu: A mechanistic review

Yaribeygi, Habib; Sathyapalan, Thozhukat; Maleki, Mina; Jamialahmadi, Tannaz; Sahebkar, Amirhossein

Authors

Habib Yaribeygi

Thozhukat Sathyapalan

Mina Maleki

Tannaz Jamialahmadi

Amirhossein Sahebkar



Abstract

Sodium-glucose co-transporter-2 inhibitors (SGLT2i) are a relatively newer class of anti-hyperglycemic medications that reduce blood glucose by inhibition of renal glucose re-uptake, thereby increasing urinary glucose excretion. Although glycosuria is the primary mechanism of action of these agents, there is some evidence suggesting they can reduce insulin resistance and induce peripheral insulin sensitivity. Identifying the molecular mechanisms by which these medications improve glucose homeostasis can help us to develop newer forms of SGLT2i with lesser side effects. We have reviewed the molecular mechanisms and signaling pathways by which SGLT2i therapy improve insulin sensitivity and ameliorates insulin resistance.

Journal Article Type Article
Publication Date 2020-01
Journal Life Sciences
Print ISSN 0024-3205
Publisher Elsevier
Peer Reviewed Peer Reviewed
Volume 240
Article Number 117090
APA6 Citation Yaribeygi, H., Sathyapalan, T., Maleki, M., Jamialahmadi, T., & Sahebkar, A. (2020). Molecular mechanisms by which SGLT2 inhibitors can induce insulin sensitivity in diabetic milieu: A mechanistic review. Life Sciences, 240, https://doi.org/10.1016/j.lfs.2019.117090
DOI https://doi.org/10.1016/j.lfs.2019.117090
Keywords Sodium-glucose co-transporter-2 inhibitors; Insulin sensitivity; Insulin resistance; Diabetes mellitus; Oxidative stress; Inflammatory response
Publisher URL https://www.sciencedirect.com/science/article/pii/S0024320519310173?via%3Dihub
Additional Information This article is maintained by: Elsevier; Article Title: Molecular mechanisms by which SGLT2 inhibitors can induce insulin sensitivity in diabetic milieu: A mechanistic review; Journal Title: Life Sciences; CrossRef DOI link to publisher maintained version: https://doi.org/10.1016/j.lfs.2019.117090; Content Type: article; Copyright: © 2019 Published by Elsevier Inc.