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残余C肽分泌对胰岛素依赖型糖尿病患者精氨酸血管加压素对低血糖和胃复安反应的影响。

Influence of residual C-peptide secretion on the arginine vasopressin response to hypoglycaemia and metoclopramide in insulin-dependent diabetes.

作者信息

Chiodera P, Volpi R, Capretti L, Speroni G, Caffarri G, Colla R, Caiazza A, Coiro V

机构信息

Department of Internal Medicine, University of Parma, Italy.

出版信息

Eur J Clin Invest. 1995 Aug;25(8):568-73. doi: 10.1111/j.1365-2362.1995.tb01747.x.

Abstract

Arginine vasopressin (AVP) hypersecretion in response to metoclopramide or to insulin-induced hypoglycaemia has been described in type I diabetes mellitus. In the present study, we examined whether residual endogenous insulin secretion may play a role in the control of this abnormal AVP secretory pattern. For this purpose, 21 insulin-dependent diabetic men and 10 age- and weight-matched normal men were tested with MCP (20 mg in an i.v. bolus). On a different occasion, subjects were tested with insulin (0.15 IU kg-1). The diabetic patients were subdivided into C-peptide negative patients (CpN, 11 patients without detectable endogenous pancreatic beta cell activity) (group I) and C-peptide positive patients (CpP, 10 patients with residual endogenous insulin secretion) (group II). Experiments started after optimization of the metabolic status of the diabetic men by 3 days of treatment with continuous subcutaneous insulin infusion. The basal concentrations of AVP were similar in all groups. The administration of MCP induced a striking elevation in plasma AVP levels in the normal controls and in the diabetic subjects of groups I and II. However, the AVP rise was significantly higher in group I and group II than in normal controls. Furthermore, group I diabetics showed higher AVP increments than group II. Insulin induced a similar hypoglycaemic nadir in all subjects at 30 min, even though the diabetic subjects of groups I and II had a delayed recovery in blood glucose levels. The hypoglycaemic pattern was similar in group I and II. Hypoglycaemia induced a striking AVP increase in the normal controls.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

在1型糖尿病患者中,已发现其对甲氧氯普胺或胰岛素诱导的低血糖会出现精氨酸加压素(AVP)分泌过多的情况。在本研究中,我们检测了残余内源性胰岛素分泌是否在这种异常AVP分泌模式的控制中发挥作用。为此,对21名胰岛素依赖型糖尿病男性和10名年龄及体重匹配的正常男性进行了甲氧氯普胺(静脉推注20毫克)测试。在另一个时间点,对受试者进行了胰岛素(0.15国际单位/千克)测试。糖尿病患者被分为C肽阴性患者(CpN,11名患者未检测到内源性胰腺β细胞活性)(第一组)和C肽阳性患者(CpP,10名患者有残余内源性胰岛素分泌)(第二组)。在通过连续皮下胰岛素输注治疗3天优化糖尿病男性的代谢状态后开始实验。所有组的AVP基础浓度相似。甲氧氯普胺给药后,正常对照组以及第一组和第二组糖尿病受试者的血浆AVP水平均显著升高。然而,第一组和第二组的AVP升高幅度明显高于正常对照组。此外,第一组糖尿病患者的AVP升高幅度高于第二组。胰岛素在30分钟时使所有受试者出现相似的低血糖最低点,尽管第一组和第二组糖尿病受试者的血糖水平恢复延迟。第一组和第二组的低血糖模式相似。低血糖在正常对照组中引起AVP显著增加。(摘要截断于400字)

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