TAK-875 Mitigates -Cell Lipotoxicity-Induced Metaflammation Damage through Inhibiting the TLR4-NF-B Pathway.

Metabolic inflammatory damage, characterized by Toll-like receptor 4 (TLR4) signaling activation, is a major mechanism underlying lipotoxicity-induced -cell damage. The present study is aimed at determining whether G protein-coupled receptor 4 (GPR40) agonist can improve -cell lipotoxicity-induced damage by inhibiting the TLR4-NF-B pathway. Lipotoxicity, inflammation-damaged -cells, obese SD, and TLR4 rat models were used in the study.