Regulation of hepatic and mucosal 6-phosphofructo-1-kinase activity by trigonella foenum-graecum linn (fenugreek) seeds of streptozotocin-induced diabetic rats

Background: Trigonella foenum-graecum Linn. (fenugreek) can ameliorate hyperglycemia and dyslipidemia, however, the detailed mechanism is unclear. The present study aims to investigate the effect of fenugreek seeds water extract (FSE) on 6-phosphofructo-1-kinase (PFK-1) activity, a key enzyme of glycolysis, in the liver and small intestine of streptozotocin induced diabetic rats and its impact on plasma glucose and lipid concentrations. Methods: 50 male Wistar rats were used in this study. The rats were divided into five groups with 10 rats in each group: normal control rats (Group1), streptozotocin-induced diabetic rats (Group2), streptozotocin-induced diabetic rats + Fenugreek seeds (0.5g/500 ml water) (Group3), streptozotocin-induced diabetic rats + Fenugreek seeds (1.0g/500 ml water) (Group4), streptozotocin-induced diabetic rats + insulin (Group5). Blood samples were then collected after the period of treatment for the analysis of glucose, total cholesterol, triacylglycerol and insulin concentration. PFK-1 for liver and intestinal mucosa was extracted and assayed. Results: Diabetic rats showed significantly lower liver and intestinal mucosa PFK-1 activities (both at P<0.05) compared with control rats. Diabetic rats treated with FSE (1.0g / 500 ml water) showed a significant (P<0.0001) increase in the PFK-1 activity of liver and intestinal mucosa by 54% and 75% respectively. The plasma glucose concentrations of diabetic rats treated with 0.5g and 1.0g fenugreek / 500 ml water were significantly (P<0.001) decreased by 32% and 43%. In addition the concentrations of plasma total cholesterol and triacylglycerol were significantly (both at P<0.0001) decreased by 57% and 42%, respectively in rats treated with 1.0g fenugreek / 500 ml water, compared with non-treated diabetic rats. Conclusions: These results may suggest that the in-vivo hypoglycaemic effect of FSE is mediated, at least in part, by the activation of PFK-1 in intestinal and liver cells.