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Protective effects of metformin on pancreatic β-cell ferroptosis in type 2 diabetes in vivo. | LitMetric

Protective effects of metformin on pancreatic β-cell ferroptosis in type 2 diabetes in vivo.

Biomed Pharmacother

School of Pharmacy, Anhui Innovative Center for Drug Basic Research of Metabolic Diseases, Wannan Medical College, Wuhu 241002, China. Electronic address:

Published: December 2023

AI Article Synopsis

Article Abstract

Metformin (Met) is the recommended first-line therapeutic drug for type 2 diabetes mellitus (T2DM) and exerts protective effects on β-cell damage. Ferroptosis, a new form of cell death, is associated with pancreatic islet injury in patients with T2DM. However, the protective effects of Met treatment against β-cell damage through ferroptosis modulation remain under-reported. This study investigated the in vivo effects of Met treatment on pancreatic β-cell ferroptosis using two different diabetic mouse models, namely, low-dose streptozotocin (STZ) and high-fat diet (HFD)-induced diabetic mice and db/db mice. Met treatment significantly restored insulin release, reduced cell mortality, and decreased the overproduction of lipid-related reactive oxygen species in the islets of both STZ/HFD-induced diabetic mice and db/db mice. Administration of the Ras-selective lethal 3 injection significantly attenuated the antiferroptosis effects of Met. Mechanistically, Met treatment alleviated β-cell ferroptosis in T2DM, which was associated with the regulation of the GPX4/ACSL4 axis in the islets. In conclusion, our findings highlight the significance of ferroptosis in T2DM β-cell damage and provide novel insights into the protective effects of Met against islet β cells.

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Source
http://dx.doi.org/10.1016/j.biopha.2023.115835DOI Listing

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