Metformin Reduces Lipotoxicity-Induced Meta-Inflammation in β-Cells through the Activation of GPR40-PLC-IP3 Pathway

Abstract EN

Background and Purpose.

Metformin, a widely used antidiabetic drug, has been shown to have anti-inflammatory properties; nevertheless, its influence on β-cell meta-inflammation remains unclear.

The following study investigated the effects of metformin on meta-inflammatory in β-cells and whether the underlying mechanisms were associated with the G protein-coupled receptor 40-phospholipase C-inositol 1, 4, 5-trisphosphate (GPR40-PLC-IP3) pathway.

Materials and Methods.

Lipotoxicity-induced β-cells and the high-fat diet-induced obese rat model were used in the study.

Results.

Metformin-reduced lipotoxicity-induced β-cell meta-inflammatory injury was associated with the expression of GPR40.

GPR40 was involved in metformin reversing metabolic inflammation key marker TLR4 activation-mediated β-cell injury.

Furthermore, downstream signaling protein PLC-IP3 of GPR40 was involved in the protective effect of metformin on meta-inflammation, and the above process of metformin was partially regulated by AMPK activity.

In addition, the anti-inflammatory effects of metformin were observed in obese rats.

Conclusion.

Metformin can reduce lipotoxicity-induced meta-inflammation in β-cells through the regulation of the GPR40-PLC-IP3 pathway and partially via the regulation of AMPK activity.