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8. Cover Image

Author

Le, Yunyi, primary, Yang, Jin, additional, Li, Fei, additional, Jiang, Yafei, additional, Wei, Tianjiao, additional, Wang, Dandan, additional, Wang, Kangli, additional, Cui, Xiaona, additional, Lin, Xiafang, additional, Yang, Kun, additional, Hong, Tianpei, additional, and Wei, Rui, additional

Published
2023
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11. Dapagliflozin improves pancreatic islet function by attenuating microvascular endothelial dysfunction in type 2 diabetes.

Author

Le, Yunyi, Yang, Jin, Li, Fei, Jiang, Yafei, Wei, Tianjiao, Wang, Dandan, Wang, Kangli, Cui, Xiaona, Lin, Xiafang, Yang, Kun, Hong, Tianpei, and Wei, Rui

Subjects
DAPAGLIFLOZIN, SODIUM-glucose cotransporters, TYPE 2 diabetes, ISLANDS of Langerhans, MICROCIRCULATION disorders, ENDOTHELIUM diseases, CELL physiology
Abstract

Aims: Sodium‐glucose co‐transporter 2 inhibitors, including dapagliflozin, improve ß cell function in type 2 diabetic individuals. Whether dapagliflozin can protect islet microvascular endothelial cells (IMECs) and thus contribute to the improvement of ß cell function remains unknown. Materials and Methods: The db/db mice were treated with dapagliflozin or vehicle for 6 weeks. ß cell function, islet capillaries and the levels of inflammatory chemokines in IMECs were detected. The mouse IMEC cell line MS‐1 cells were incubated with palmitate and/or dapagliflozin for 24 h. Angiogenesis and inflammatory chemokine levels were evaluated, and the involved signalling pathways were analysed. The mouse ß cell line MIN6 cells, in the presence or absence of co‐culture with MS‐1 cells, were treated with palmitate and/or dapagliflozin for 24 h. The expression of ß cell specific markers and insulin secretion in MIN6 cells were determined. Results: Dapagliflozin significantly improved ß cell function, increased islet capillaries and decreased the levels of inflammatory chemokines of IMECs in db/db mice. In the palmitate‐treated MS‐1 cells, angiogenesis was enhanced and the levels of inflammatory chemokines were downregulated by dapagliflozin. Either a PI3K inhibitor or mTOR inhibitor eliminated the dapagliflozin‐mediated effects. Importantly, dapagliflozin attenuated the palmitate‐induced downregulation of ß cell function‐related gene expression and insulin secretion in MIN6 cells co‐cultured with MS‐1 cells but not in those on mono‐culture. Conclusions: Dapagliflozin restores islet vascularisation and attenuates the inflammation of IMECs in type 2 diabetic mice. The dapagliflozin‐induced improvement of ß cell function is at least partially accounted for by its beneficial effects on IMECs in a PI3K/Akt‐mTOR‐dependent manner. [ABSTRACT FROM AUTHOR]

Published
2023
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