OBJECTIVE: To investigate the effect of Supplemented Taohe Chengqi Decoction (STHCQD) in treating non-insulin dependent diabetes mellitus (NIDDM). METHODS: The model of rats with NIDDM was formed with injection of streptozotocin and fed on high calorie diet to study the effects of STHCQD on the release of insulin mediator from liver cell membranes, the glucose oxidation in adipocytes as well as the insulin sensitivity. RESULTS: (1) Fasting serum glucose, serum insulin, intake of food and water were significantly decreased (P < 0.05-0.01) in STHCQD-treated diabetic rats as compared with untreated diabetic rats, while the insulin sensitivity was significantly increased (P < 0.05). (2) The liver cell membranes from STHCQD-treated diabetic rats released the quantity of insulin receptor which inhibited adenylate cyclase activity, but this effect was blunted in untreated diabetic rats (P < 0.05). (3) A significantly increased glucose oxidation in adipocyte of STHCQD-treated diabetic rats was found as compared with those of untreated diabetic rats (P < 0.05). CONCLUSIONS: STHCQD therapy increased sensitivity and responsiveness of target cells to insulin, i.e., it might decrease insulin resistance at receptor sites and postreceptor sites in rats with NIDDM, but could not reverse the insulin resistance.
OBJECTIVE: To investigate the effect of Supplemented Taohe Chengqi Decoction (STHCQD) in treating non-insulin dependent diabetes mellitus (NIDDM). METHODS: The model of rats with NIDDM was formed with injection of streptozotocin and fed on high calorie diet to study the effects of STHCQD on the release of insulin mediator from liver cell membranes, the glucose oxidation in adipocytes as well as the insulin sensitivity. RESULTS: (1) Fasting serum glucose, serum insulin, intake of food and water were significantly decreased (P < 0.05-0.01) in STHCQD-treated diabeticrats as compared with untreated diabeticrats, while the insulin sensitivity was significantly increased (P < 0.05). (2) The liver cell membranes from STHCQD-treated diabeticrats released the quantity of insulin receptor which inhibited adenylate cyclase activity, but this effect was blunted in untreated diabeticrats (P < 0.05). (3) A significantly increased glucose oxidation in adipocyte of STHCQD-treated diabeticrats was found as compared with those of untreated diabeticrats (P < 0.05). CONCLUSIONS: STHCQD therapy increased sensitivity and responsiveness of target cells to insulin, i.e., it might decrease insulin resistance at receptor sites and postreceptor sites in rats with NIDDM, but could not reverse the insulin resistance.