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首页> 外文期刊>Metabolism: Clinical and Experimental >Effects of glucagon on postprandial carbohydrate metabolism in nondiabetic humans.
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Effects of glucagon on postprandial carbohydrate metabolism in nondiabetic humans.

机译:胰高血糖素对非糖尿病人餐后碳水化合物代谢的影响。

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The present experiments sought to determine whether glucagon concentrations mimicking those observed in people with diabetes mellitus alter postprandial carbohydrate metabolism in nondiabetic humans. We measured the gastric emptying of solids and liquids, the systemic rate of appearance of ingested glucose, and endogenous glucose production either when postprandial suppression of glucagon was prevented by infusing glucagon at a rate of 0.65 ng/kg/min, when postprandial glucagon concentrations were elevated by infusing glucagon at a rate of 3.0 ng/kg/min, or when postprandial suppression of glucagon was permitted by infusion of saline. Despite marked differences in glucagon concentrations, postprandial glucose and insulin concentrations did not differ on any occasion. Although gastric emptying of liquids and solids was comparable on all three occasions, the high-dose, but not the low-dose, glucagon infusion caused a slight delay in the systemic appearance of ingested glucose and a significant decrease (P < .01) in postprandial D-xylose concentrations, suggesting a delay in carbohydrate absorption. However, this was offset by an increase (P < .05) in endogenous glucose production, resulting in no difference in postprandial glucose appearance. We conclude that in the absence of insulin deficiency, neither a lack of suppression of glucagon nor an elevation of glucagon to levels encountered in uncontrolled diabetes mellitus cause postprandial hyperglycemia in nondiabetic humans.
机译:本实验试图确定与非糖尿病人中餐后碳水化合物代谢有关的胰高血糖素浓度是否能模拟糖尿病人中观察到的浓度。我们测量了通过以0.65 ng / kg / min的速度注入胰高血糖素来防止餐后胰高血糖素的抑制而在餐后胰高血糖素浓度为0.05的情况下预防胃内的固体和液体排空,摄入葡萄糖的全身出现率以及内源性葡萄糖生成。通过以3.0 ng / kg / min的速度注入胰高血糖素,或在餐后通过注入生理盐水抑制胰高血糖素而使胰高血糖素升高。尽管胰高血糖素浓度存在明显差异,但餐后葡萄糖和胰岛素浓度在任何情况下均没有差异。尽管在所有三种情况下胃液和固体的排空情况均相当,但大剂量胰高血糖素输注而不是小剂量胰高血糖素输注会引起葡萄糖摄入的全身出现轻微延迟,并显着降低(P <.01)。餐后D-木糖浓度升高,提示碳水化合物吸收延迟。但是,这被内源性葡萄糖产量的增加(P <0.05)所抵消,导致餐后葡萄糖外观无差异。我们得出的结论是,在没有胰岛素缺乏的情况下,缺乏抑制胰高血糖素的作用或升高胰高血糖素至不受控制的糖尿病中所遇到的水平都不会在非糖尿病患者中引起餐后高血糖。

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