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肥胖症患者胰腺多肽对促胰液素的反应:葡萄糖不耐受的影响

Pancreatic polypeptide response to secretin in obesity: effects of glucose intolerance.

作者信息

Glaser B, Zoghlin G, Pienta K, Vinik A I

机构信息

Department of Internal Medicine (Division of Endocrinology and Metabolism), University of Michigan Medical Center, Ann Arbor.

出版信息

Horm Metab Res. 1988 May;20(5):288-92. doi: 10.1055/s-2007-1010817.

DOI:10.1055/s-2007-1010817
PMID:3042579
Abstract

Pancreatic polypeptide (PP) may function as a regulator of satiety. Its secretion is impaired in certain animal models of obesity and the administration of PP may improve the hyperphagia and hyperinsulinism seen in these animals. In obese humans, decreased, normal or increased, basal and stimulated concentrations of PP in plasma have been reported. However the advent of diabetes confounds the picture since PP levels in diabetes are generally raised. We have therefore examined the PP responses to intravenous secretin, a known PP secretagogue, in 23 obese subjects, 12 with normal and 11 with abnormal glucose tolerance, and compared the results with those in 23 age and sex-matched healthy controls. The mean maximum PP level in obese subjects with normal glucose tolerance (98 +/- 13 pg/ml) was significantly less than that in normal subjects (218 +/- 23 pg/ml) but in obese subjects with abnormal glucose tolerance, it was significantly greater (578 +/- 115 pg/ml). Within each of the 3 study groups taken separately, PP response to secretin was not correlated with glucose or insulin levels, or with the degree of obesity. Thus, obesity per se appears to be associated with impaired PP responses, which may be masked by abnormalities in glucose tolerance.

摘要

胰多肽(PP)可能起到饱腹感调节剂的作用。在某些肥胖动物模型中,其分泌受损,给予PP可改善这些动物出现的摄食过多和高胰岛素血症。在肥胖人类中,血浆PP的基础浓度和刺激浓度有降低、正常或升高的报道。然而,糖尿病的出现使情况变得复杂,因为糖尿病患者的PP水平通常会升高。因此,我们检测了23名肥胖受试者(12名糖耐量正常,11名糖耐量异常)对静脉注射促胰液素(一种已知的PP促分泌剂)的反应,并将结果与23名年龄和性别匹配的健康对照者进行比较。糖耐量正常的肥胖受试者的平均最大PP水平(98±13 pg/ml)显著低于正常受试者(218±23 pg/ml),但糖耐量异常的肥胖受试者的平均最大PP水平则显著更高(578±115 pg/ml)。在分别进行的3个研究组中,PP对促胰液素的反应与血糖或胰岛素水平以及肥胖程度均无相关性。因此,肥胖本身似乎与PP反应受损有关,而这可能被糖耐量异常所掩盖。

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