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

Figure 4

The protective effect of metformin was partially independent of AMPK activity. (a) Metformin concentration-dependently increased the expression of AMPK. (A1) Representative Western blot images for each group. (A2) The ratio of target protein to β-actin. (b–e) The relationship between metformin-regulated lipotoxicity and AMPK inhibitor. (b) The rate of apoptosis in β-cells. (c) Levels of BIS and GSIS. (d) Expression of IP3 in β-cells. (e) Expression levels of TLR4, NF-κB subunit P65, and GPR40. (f–i) Effect of AICAR on PA-induced β-cell injury. (f) The rate of apoptosis in β-cells. (g) Levels of BIS and GSIS. (h) Expression of IP3 in β-cells. (i) Expression levels of TLR4, NF-κB subunit P65, and GPR40. (a) ^A vs. NC group (without PA and MF), ^B vs. 0.5 mmol/L PA group, ^C vs. 0.5 mmol/L PA+25 μmol/L MF group, and ^D vs. 0.5 mmol/L PA+50 μmol/L MF group. (b–e) ^A vs. NC group, ^B vs. 0.5 mmol/L PA+100 μmol/L MF group, and ^C vs. 10 μmol/L compound C group. (f–i) ^A vs. NC group, ^B vs. 1.0 mmol/L AICAR group, and ^C vs. 0.5 mmol/L PA+1.0 mmol/L AICAR group.

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