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胰岛素受体在噻嗪类药物诱导糖耐量机制中的可能作用。

Possible role for insulin receptors in the mechanism of thiazide induced glucose tolerance.

作者信息

Gill J S, Al-Hussary N, Atkins T W, Taylor K G, Beevers D G

出版信息

J Hypertens Suppl. 1984 Dec;2(3):S573-6.

PMID:6599719
Abstract

The role of cellular insulin receptors in the mechanism of thiazide induced glucose intolerance was studied in 10 non-diabetics and six diet controlled type II diabetics with mild essential hypertension. Glucose tolerance tests (75 g) were performed at the start of the study, after one month of placebo and after one month on bendrofluazide 5 mg daily. Erythrocyte insulin receptor status was measured on each occasion in the fasting state. In non-diabetics, low affinity insulin receptor concentration increased after bendrofluazide but high affinity receptor concentration remained unchanged. In the diabetics, there was no change in either high or low affinity insulin receptor concentration. No change in insulin receptor affinity occurred in either group. In the long term, non-diabetics may maintain normal glucose tolerance on thiazide diuretics by increasing insulin receptor numbers. This adjustment did not occur in diabetic patients which may explain the deterioration in glucose tolerance.

摘要

在10名非糖尿病患者和6名采用饮食控制的轻度原发性高血压II型糖尿病患者中,研究了细胞胰岛素受体在噻嗪类药物诱发葡萄糖耐量异常机制中的作用。在研究开始时、服用安慰剂1个月后以及每天服用5毫克苄氟噻嗪1个月后,进行葡萄糖耐量试验(75克)。每次均在空腹状态下测量红细胞胰岛素受体状态。在非糖尿病患者中,苄氟噻嗪治疗后低亲和力胰岛素受体浓度增加,但高亲和力受体浓度保持不变。在糖尿病患者中,高亲和力和低亲和力胰岛素受体浓度均无变化。两组患者的胰岛素受体亲和力均未发生变化。从长远来看,非糖尿病患者可能通过增加胰岛素受体数量来维持噻嗪类利尿剂治疗下的正常葡萄糖耐量。糖尿病患者未出现这种调节情况,这可能解释了葡萄糖耐量的恶化。

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