Journal of acupuncture and meridian studies · 2009
Increase in plasma glucose lowering action of rosiglitazone by electroacupuncture at bilateral Zusanli acupoints (ST.36) in rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Pai Hui-Ching, Tzeng Chung-Yuh, Lee Yu-Chen, Chang Chin-Hsien, Lin Jaung-Geng, Cheng Juei-Tang, Chang Shih-Liang
Аннотация
OBJECTIVES: Hypoglycemia induced by electroacupuncture (EA) is due to an increase of insulin secretion and/or mediation of beta-endorphin. We applied EA at the Zusanli (ST.36) acupuncture point (acupoint) in combination with rosiglitazone (TZD) administration to evaluate their effect on plasma glucose and to explore possible mechanisms of action.
METHODS: Thirty six normal adult Wistar rats were randomly divided into four groups: the 0.1 mg/kg TZD group (0.1TZD), 0.1 mg/kg TZD and EA group (0.1TZD + EA), EA group, and control group. In other experiments, streptozotocin was used to induce type 2 diabetes mellitus in neonatal rats; these were then randomly divided into a 0.1TZD group, 0.1TZD + EA group, and EA group and changes in plasma glucose and insulin concentrations evaluated.
RESULTS: A marked hypoglycemic response was observed in the normal rat 0.1TZD, 0.1TZD + EA and EA groups, with the response more significant in the 0.1TZD + EA group than in the 0.1TZD group. Among the diabetic animals, the hypoglycemic responses in the 0.1TZD + EA and EA groups were greater than in the 0.1TZD group. In both the normal and diabetic rats, insulin secretion was increased by EA or 0.1TZD + EA treatment, but not by 0.1TZD.
CONCLUSIONS: The plasma glucose lowering action of rosiglitazone was increased by EA in both normal and diabetic rats, indicating that the application of EA may enhance the hypoglycemic action of this insulin sensitizer.
METHODS: Thirty six normal adult Wistar rats were randomly divided into four groups: the 0.1 mg/kg TZD group (0.1TZD), 0.1 mg/kg TZD and EA group (0.1TZD + EA), EA group, and control group. In other experiments, streptozotocin was used to induce type 2 diabetes mellitus in neonatal rats; these were then randomly divided into a 0.1TZD group, 0.1TZD + EA group, and EA group and changes in plasma glucose and insulin concentrations evaluated.
RESULTS: A marked hypoglycemic response was observed in the normal rat 0.1TZD, 0.1TZD + EA and EA groups, with the response more significant in the 0.1TZD + EA group than in the 0.1TZD group. Among the diabetic animals, the hypoglycemic responses in the 0.1TZD + EA and EA groups were greater than in the 0.1TZD group. In both the normal and diabetic rats, insulin secretion was increased by EA or 0.1TZD + EA treatment, but not by 0.1TZD.
CONCLUSIONS: The plasma glucose lowering action of rosiglitazone was increased by EA in both normal and diabetic rats, indicating that the application of EA may enhance the hypoglycemic action of this insulin sensitizer.