| Résumé | The plant alkaloid berberine (BBR) has been reported to have antidiabetic effect in humans and animals. However, the mechanism of action is not well understood. The present study was conducted to determine the effect and mechanism of action of BBR on the free-fatty-acid (FFA)–induced insulin resistance in muscle cells. The FFA-induced insulin-resistant cell model was established in L6 myotubes by treating them with 250 μmol/L of palmitic acid. The inclusion of FFA in the medium increased peroxisome proliferator–activated receptor γ (PPARγ) and fatty acid transferase (FAT/CD36) expressions by 26% and 50% and decreased glucose consumption by 43% and insulin-mediated glucose uptake by 63%, respectively. Berberine treatment increased the glucose consumption and insulin-stimulated glucose uptake in normal cells and improved glucose uptake in the FFA-induced insulin-resistant cells. The improved glucose uptake by BBR was accompanied with a dose-dependent decrease in PPARγ and FAT/CD36 protein expressions. In insulin-resistant myotubes, BBR (5 μmol/L) decreased PPARγ and FAT/CD36 proteins by 31% and 24%, whereas PPARγ antagonist GW9662 reduced both proteins by 56% and 46%, respectively. In contrast, PPARγ agonist rosiglitazone increased the expression of PPARγ and FAT/CD36 by 34% and 21%, respectively. Our results suggest that BBR improves the FFA-induced insulin resistance in myotubes through inhibiting fatty acid uptake at least in part by reducing PPARγ and FAT/CD36 expressions. |
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