A role for alpha-adrenergic receptors in abnormal insulin secretion in diabetes mellitus.
A role for alpha-adrenergic receptors in abnormal insulin secretion in diabetes mellitus.
复制标题
α-肾上腺素能受体在糖尿病胰岛素分泌异常中的作用。
DOI：
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发表时间：
1976
影响因子：
15.9
通讯作者：
D. Porte
中科院分区：
文献类型：
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作者：
R. Robertson;Jeffrey B. Halter;D. Porte
为了确定内源性α -肾上腺素能活性是否与非酮症、高血糖、糖尿病患者的胰岛素分泌异常有关，我们对正常和糖尿病受试者进行了α -肾上腺素能阻断。静脉注射酚妥拉明1 h后，糖尿病患者循环胰岛素水平明显高于正常对照组（P < 0.01）。在酚妥拉明输注期间，正常受试者（P < 0.05）和糖尿病患者（P < 0.02）对静脉注射葡萄糖（20 g）脉冲的急性胰岛素反应也显著增强；糖尿病患者的这种增加是糖尿病患者的5倍。同时使用-肾上腺素能阻滞剂心得安并没有改变这些结果。因此，内源性α -肾上腺素能活性在糖尿病患者胰岛素分泌异常中的作用被提出。为了确定这种肾上腺素能活性是否与循环儿茶酚胺升高有关，我们比较了静脉注射葡萄糖脉冲的正常和非酮症糖尿病患者血浆儿茶酚胺水平。与正常组相比，糖尿病组在血糖脉冲前的这些水平显著升高（P < 0.02），而在血糖脉冲后两组的水平均显著升高（P分别小于0.02和0.001）。这些数据表明，过量的儿茶酚胺分泌可能导致内源性α -肾上腺素能活性异常，从而导致糖尿病患者胰岛素分泌缺陷。
To determine whether endogenous alpha-adrenergic activity contributes to abnormal insulin secretion in nonketotic, hyperglycemic, diabetic patients, alpha-adrenergic blockade was produced in normal and diabetic subjects. The diabetics had a significantly (P less than 0.01) greater increase in circulating insulin 1 h after an intravenous phentolamine infusion than did the normal subjects. During the phentolamine infusion, there was also a significant augmentation of acute insulin responses to intravenous glucose (20 g) pulses in normal subjects (P less than 0.05) and diabetics (P less than 0.02); this augmentation was fivefold greater in the diabetics. Simultaneous treatment with the beta-adrenergic blocking agent, propranolol, did not alter these findings. Thus a role for exaggerated endogenous alpha-adrenergic activity in abnormal insulin secretion of the diabetic subjects is suggested. To determine whether this alpha-adrenergic activity might be related to elevated circulating catecholamines, total plasma-catecholamine levels were compared in normal and nonketotic diabetic subjects given intravenous glucose pulses. These levels were significantly greater (P less than 0.02) in the diabetic compared to the normal group before the glucose pulse, and increased significantly in both groups (P less than 0.02 and less than 0.001, respectively) after the pulse. These data suggest that excessive catecholamine secretion may lead to an abnormal degree of endogenous alpha-adrenergic activity, which contributes to defective insulin secretion in diabetic subjects.