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口服葡萄糖负荷后生长抑素的抗糖尿病作用:是由于抑制胰高血糖素和生长激素还是抑制肠道碳水化合物吸收?

Antidiabetic action of somatostatin after oral glucose loading: due to suppression of glucagon and growth hormone or of intestinal carbohydrate absorption?

作者信息

Bratusch-Marrain P, Vierhapper H, Grubeck-Loebenstein B, Waldhäusl W, Nowotny P

出版信息

Horm Metab Res. 1981 Jun;13(6):305-9. doi: 10.1055/s-2007-1019253.

Abstract

To elucidate the mechanism by which somatostatin lowers blood glucose concentration and insulin requirement following carbohydrate ingestion in insulin dependent diabetic patients (IDDM; n = 6), the amount of insulin required for the assimilation of a 50 g glucose load was determined by means of an automated glucose-controlled insulin infusion system with and without concomitant somatostatin infusion. During the 3 hour period following glucose loading plasma concentrations of glucagon and growth hormone were diminished by somatostatin, as were the rise in blood glucose and insulin requirement (4.0 +/- 1.2 U) when compared with the control study (11.3 +/- 1.5 U; p less than 0.01). With cessation of somatostatin blood glucose levels and insulin requirement rose during the following 2 hour observation period (7.5 +/- 1.2 U) but remained basal during the control study (0.7 +/- 0.6 U; p less than 0.0005). Thus the integrated amounts of insulin required for glucose hormone were temporarily suppressed by somatostatin. It is concluded that the diminished insulin requirement and delayed rise in blood glucose during somatostatin administration after an oral glucose load is not due to its "antidiabetic" action by suppressing glucagon and growth hormone release. Our findings favour inhibition of intestinal carbohydrate absorption as the determining cause for the "antidiabetic" action of somatostatin.

摘要

为了阐明生长抑素降低胰岛素依赖型糖尿病患者(IDDM;n = 6)摄入碳水化合物后血糖浓度和胰岛素需求量的机制,通过自动血糖控制胰岛素输注系统,在有和没有同时输注生长抑素的情况下,测定同化50g葡萄糖负荷所需的胰岛素量。在葡萄糖负荷后的3小时内,生长抑素使胰高血糖素和生长激素的血浆浓度降低,与对照研究(11.3±1.5U)相比,血糖升高和胰岛素需求量(4.0±1.2U)也降低(p<0.01)。停止输注生长抑素后,在接下来的2小时观察期内血糖水平和胰岛素需求量升高(7.5±1.2U),但在对照研究期间保持在基础水平(0.7±0.6U;p<0.0005)。因此,生长抑素暂时抑制了葡萄糖激素所需胰岛素的总量。得出的结论是,口服葡萄糖负荷后给予生长抑素期间胰岛素需求量减少和血糖升高延迟,并非由于其通过抑制胰高血糖素和生长激素释放而产生的“抗糖尿病”作用。我们的研究结果支持抑制肠道碳水化合物吸收是生长抑素“抗糖尿病”作用的决定性原因。

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