Hypoglycemic effect of Chrysanthemum morifolium extract on alloxan-induced diabetic mice is associated with peroxisome proliferator-activated receptor α/γ-mediated hepatic glycogen synthesis

Previous studies have indicated that polyphenol-rich Chrysanthemum morifolium extract (CME) may inhibit the formation of hyperlipidemic fatty liver in mice. But there has been no report about therapeutic effect on diabetes mellitus. In the present study, we investigated the action of CME and its potential mechanisms. A mouse model with diabetes mellitus was induced by alloxan. The results showed that after treatment of diabetic mice with polyphenol-rich CME 150 and 300 mg/kg for 6 weeks, the levels of fasting blood glucose (FBG) as well as water and food consumption were decreased (P < 0.05 or P < 0.01), the content of hepatic glycogen was increased, especially in the 300 mg/kg group (P < 0.05), but no significant variations in the body-weight gain, fasting serum insulin, and muscular glycogen were observed. Importantly, toxic alloxan treatment might decrease the protein expressions of hepatic peroxisome proliferator-activated receptor (PPAR) α/γ, glycogen synthase (GS), and glucose transporter-2 (Glut-2) (P < 0.05 or P < 0.01), while CME might reverse the changes (P < 0.01). These findings demonstrate that the reduction of PPARα/γ-mediated hepatic glycogen synthesis may involve in the alloxan-induced hyperglycemia, and the hypoglycemic mechanisms of CME may be mainly associated with the increment of hepatic glycogen synthesis via upregulation of PPARα/γ-mediated GS and Glut-2 protein expressions.