A preliminary investigation of the mechanisms underlying the effect of berberine in preventing high-fat diet-induced insulin resistance in rats.

Berberine exerts insulin resistance-improving effects, the underlying mechanism of which is not well understood. We herein aimed to examine the effects of berberine on mediators of insulin signaling in pancreatic β- and α- islet cells and hepatocytes using a rat obesity model. Rats were fed the following diets for 22 weeks: normal control (NC); normal+berberine (NC+BBR 200 mg/kg/day); high-fat (HF); HF+BBR(1) (BBR 100 mg/kg/day); HF+BBR(2) (BBR 200 mg/kg/day). Metabolic parameters were assessed and mediators of insulin signaling were quantified by immunohistochemistry. The HF diet significantly increased body weight (BW), visceral fat (VF), the visceral fat to BW ratio (VF/BW), and insulin resistance index in the HF group compared with the NC group. Both doses of BBR significantly reduced HF diet-induced increases in BW, VF, and VF/BW. IR and IRS-1 expression in β-cells was significantly lower in the HF group, but not the HF+BBR groups, compared with the NC and NC+BBR groups. Glucagon expression in α-cells was significantly higher in the HF group compared with all other groups. IR expression in α-cells was significantly lower in the HF group compared with the NC, NC+BBR, and HF+BBR(2) groups. IR expression in hepatocytes was significantly lower in the HF group compared with all groups. Our preliminary findings suggest that berberine may ameliorate the development of insulin resistance by differentially preventing alterations in expression of IR, IRS-1, and glucagon in β-cells, α-cells, and hepatocytes.