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β-肾上腺素能阻滞剂在抑制1型(胰岛素依赖型)糖尿病中肾上腺素诱导的葡萄糖生成方面更有效。

Beta-adrenergic blockade is more effective in suppressing adrenaline-induced glucose production in Type 1 (insulin-dependent) diabetes.

作者信息

Shamoon H, Sherwin R

出版信息

Diabetologia. 1984 Mar;26(3):183-9. doi: 10.1007/BF00252404.

Abstract

To examine whether diabetes affects the ability of beta-blockade to suppress adrenaline-stimulated hepatic glucose production, we infused adrenaline with and without propranolol into normal subjects and diabetic patients receiving a constant insulin infusion in basal amounts. In normal subjects, propranolol did not block the transient 50%-60% rise in glucose production during adrenaline infusion. In contrast, propranolol virtually abolished adrenaline-induced hyperglycaemia and glucose production was virtually abolished by propranolol in the diabetic patients, even though they demonstrated an exaggerated response to adrenaline alone (persistent increase in glucose production of 50%-90% above baseline). When insulin was infused together with adrenaline and propranolol in normal subjects in doses exceeding those given to the diabetics (plasma insulin rose threefold), the rise in glucose production was still threefold greater than in the diabetic patients (p less than 0.02). We conclude that beta-blockade is more effective in suppressing the hepatic response to adrenaline in diabetics than in normal subjects. Our data may explain why diabetic subjects are more vulnerable to hypoglycaemia during treatment with propranolol.

摘要

为了研究糖尿病是否会影响β受体阻滞剂抑制肾上腺素刺激的肝脏葡萄糖生成的能力,我们在基础状态下持续输注胰岛素的正常受试者和糖尿病患者中,分别在有无普萘洛尔的情况下输注肾上腺素。在正常受试者中,普萘洛尔并未阻断肾上腺素输注期间葡萄糖生成短暂升高50%-60%。相反,普萘洛尔几乎消除了肾上腺素诱导的高血糖,并且在糖尿病患者中,普萘洛尔几乎消除了葡萄糖生成,尽管他们对单独肾上腺素的反应有所增强(葡萄糖生成持续增加至高于基线水平50%-90%)。当在正常受试者中以超过给予糖尿病患者的剂量将胰岛素与肾上腺素和普萘洛尔一起输注时(血浆胰岛素升高了三倍),葡萄糖生成的升高仍比糖尿病患者大三倍(p<0.02)。我们得出结论,β受体阻滞剂在抑制糖尿病患者肝脏对肾上腺素反应方面比在正常受试者中更有效。我们的数据可能解释了为什么糖尿病患者在使用普萘洛尔治疗期间更容易发生低血糖。

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