Abstract
Background. According to the research of epidemiologists, 171 million peoples were estimated to have Type 2 diabetes, and this is expected to increase to 366 million by 2030. There is increasing evidence indicates that excessive intake of fructose may play a role in diabetes. The first aim was to evaluate the antihyperlipidemic and antihyperglycemic effects of ginseng flower in high fructose-fed rats. Furthermore, we demonstrated the mechanism of antihyperlipidemic and antihyperglycemic effects of ginseng flower.
Methods. Ginseng flowers were extracted with hot water and dried via freeze dryer. Six ginsenosides in the extract were measured by HPLC -DAD. The extract was intragastric administered to rats during high fructose feeding period. After sixty day, all rats were sacrificed, blood were collected and their livers were homogenized. Plasma glucose levels and lipid profiles were assessed. The hepatic antioxidant makers and signal transduction were assayed by ELISA and western blot.
Results. Each gram of the extract mainly contains 1.70 mg Rb1, 3.96 mg Rg1 and 5.12 mg Rd. Sixty days after feeding with high fructose solution, higher levels of plasma glucose, triglycerides, NEFA, AST and ALT were observed. The levels of hepatic TG and the relative hepatic weight in high fructose-fed rats were higher than those in normal diet-fed rats. Furthermore, we also found that high fructose decreased the activities of hepatic antioxidant enzymes and increased hepatic MDA levels in rats. High fructose-fed rats showed lower expression of hepatic PPAR-gamma and GLUT-2 proteins but higher expression of hepatic SREBP-1c, FAS and ACC-1proteins. Ginseng flower extract could decrease plasma glucose levels and lipid profiles. It further reversed alterations of cortical antioxidant enzymes and restored the expression of hepatic PPAR-gamma and GLUT-2 proteins.
Conclusions. Ginseng flower decreased hyperlipidemia and hyperglycemia caused by high fructose feeding in rats, and the effects might be through its active components ginsenoside Rb1 and Rg1. Then these effects might be related to the decrease in hepatic oxidative damage via reversing the activities of antioxidant enzymes, and then the reversal of the expression of hepatic PPAR-gamma and GLUT-2 proteins.
