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

Figure 2

GPR40 and its involvement in metformin improves LPS-induced inflammatory injury. All data is presented as of three independent experiments. Metformin improves LPS-induced inflammatory apoptosis (a), insulin secretion disorder (b), and TLR4 and NF-κB subunit P65 expression (c). Regulation of GPR40 expression and the protective effects of metformin on LPS-induced β-cell apoptosis (d), insulin secretion disorder (e), and TLR4 and NF-κB subunit P65 expression (f). Activation of GPR40 by TAK-875 protects LPS-induced β-cell apoptosis (g), insulin secretion disorder (h), and TLR4 and NF-κB subunit P65 expression (i). Inhibition of GPR40 by DC260126 aggravated LPS-induced apoptosis (j), insulin secretion disorder (k), and TLR4 and NF-κB subunit P65 expression (l). (a–c) ^A vs. NC group (without LPS and MF), ^B vs. 1.0 mg/L LPS group, ^C vs. 1.0 mg/L LPS+25 μmol/L MF group, and ^D vs. 1.0 mg/L LPS+50 μmol/L MF group. (d–f) ^A vs. NC group (without LPS and MF), ^B vs. 1.0 mg/L LPS group, and ^C vs. 1.0 mg/L LPS+100 μmol/L MF group. (g–i) ^A vs. NC group (without LPS and TAK-875), ^B vs. TAK-875 group, and ^C vs. LPS group. (j–l) ^A vs. NC group (without LPS and DC260126), ^B vs. DC260126 group, and ^C vs. LPS group.

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