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糖尿病神经病变中胰高血糖素对低血糖的反应。

Glucagon response to hypoglycemia in diabetic neuropathy.

作者信息

Maher T D

出版信息

Horm Metab Res Suppl. 1980;9:87-9.

PMID:6929783
Abstract

Glucagon release during insulin hypoglycemia was studied in diabetics with autonomic neuropathy (N = 9), diabetics without clinical neuropathy (N =8), and normals (N = 9). With similar hypoglycemic stimulus, growth hormone and plasma cortisol increased in all groups. Plasma glucagon increased threefold in normals (121 +/- 19 vs. 308 +/- 30 pg/ml., mean +/- SEM of baseline vs. hypoglycemic peak) and twofold in nonneuropathic diabetics (128 +/- 13 vs. 209 +/- 30). There was no glucagon rise during hypoglycemia in the neuropathic diabetics (128 +/- 23 vs. 115 +/- 20). Arginine infusion produced glucagon rise in the neuropathic diabetics (106 +/- 16 vs. 523 +/- 103). The study suggests that failure to release glucagon during hypoglycemia is due to diabetic neuropathy. Neuropathy may contribute to metabolic instability.

摘要

对患有自主神经病变的糖尿病患者(N = 9)、无临床神经病变的糖尿病患者(N = 8)和正常人(N = 9)在胰岛素低血糖期间的胰高血糖素释放情况进行了研究。在相似的低血糖刺激下,所有组的生长激素和血浆皮质醇均升高。正常人的血浆胰高血糖素增加了两倍(基础值均值±标准误为121±19 pg/ml,低血糖峰值为308±30 pg/ml),无神经病变的糖尿病患者增加了一倍(128±13 vs. 209±30)。神经病变的糖尿病患者在低血糖期间胰高血糖素无升高(128±23 vs. 115±20)。精氨酸输注使神经病变的糖尿病患者的胰高血糖素升高(106±16 vs. 523±103)。该研究表明,低血糖期间胰高血糖素释放失败是由于糖尿病神经病变。神经病变可能导致代谢不稳定。

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