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低血糖对人胰多肽分泌的刺激与肾上腺素能机制无关。

Stimulation of human pancreatic polypeptide secretion by hypoglycemia is independent of adrenergic mechanisms.

作者信息

Rizza R, Go V, Cryer P, Verdonk C, Gerich J

出版信息

J Clin Endocrinol Metab. 1982 Dec;55(6):1234-6. doi: 10.1210/jcem-55-6-1234.

Abstract

Human pancreatic polypeptide (HPP) increases after insulin-induced hypoglycemia. To determine whether adrenergic mechanisms contribute to this increase in normal man, six subjects were studied on two occasions: once after insulin alone and once after insulin plus simultaneous alpha (phentolamine)- and beta (propranolol)-adrenergic blockade. Despite comparable hypoglycemia (51 +/- 4 vs. 49 +/- 4 mg/dl), the increase in HPP did not differ in the presence or absence of adrenergic blockade (721 +/- 215 vs. 736 +/- 193 pg/ml, respectively). These findings suggest that HPP secretion during hypoglycemia is not dependent on adrenergic mechanisms.

摘要

胰岛素诱导的低血糖后,人胰多肽(HPP)会增加。为了确定肾上腺素能机制是否促成正常人的这种增加,对6名受试者进行了两次研究:一次仅注射胰岛素后,另一次在注射胰岛素的同时进行α(酚妥拉明)和β(普萘洛尔)肾上腺素能阻滞。尽管低血糖程度相当(分别为51±4 vs. 49±4 mg/dl),但无论有无肾上腺素能阻滞,HPP的增加并无差异(分别为721±215 vs. 736±193 pg/ml)。这些发现表明,低血糖期间HPP的分泌不依赖于肾上腺素能机制。

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