[Protection mechanisms of hesperidin on mouse with insulin resistance].

To explore the effects of hesperidin on glycolipid metabolic disorders and its mechanism in mice induced by high-fat diet, 40 male C57 mice were randomly divided into control group, OB group, low dose group (OB+ hes-low) and high dose group (OB+ hes-high) according to the diet. After 16 weeks, the body weight, liver index and visceral fat index in all mice were detected. The glucose metabolism indications (blood glucose, insulin levels and HOMA-IR) and serum lipid levels were evaluated. The mRNA expression of insulin signaling pathway genes(IR, IRS1, Glut2, Glut4), lipid metabolism pathway genes(SREBP-1c, FAS, ACC, PPARα) and AMPK were analyzed by Real-time PCR. After 16-week feeding, the indicators in OB group were higher than those in control group, including body weight, body fat deposition, serum glucose, serum lipid, serum insulin and HOMA-IR index (P<0.05). And impaired glucose tolerance occurred in the OB group (P<0.05). Treating with hesperidin, whether in low or high dose, attenuated these changes (P<0.05), especially in high dose group(P<0.05). Hesperidin, especially in high dose, upregulated the mRNA expressions of AMPK (P<0.05), which had impact on the gene expressions of insulin signaling pathway (IR, IRS-1, Glut2/4) (P<0.05) and lipid metabolism related genes (SREBP-1c and Fas and ACC) (P<0.05). The activatory effect of hesperidin on the mRNA expressions of PPARα was also observed (P<0.05), especially in high dose group (P<0.05). Hesperidin inhibits obesity, hyperglycemia, hyperlipemia and attenuates insulin resistance. These effects might be closed related to the activation of AMPK, which regulate the insulin signaling pathway and lipid metabolism.