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患有经治疗和未经治疗的乳糜泻的成年患者的胰高血糖素样肽-2血浆浓度。

Plasma concentrations of glucagon-like peptide-2 in adult patients with treated and untreated coeliac disease.

作者信息

Caddy Grant R, Ardill Joy E S, Fillmore Davina, Caldwell Carolyn M, McKibben Bronac M, Gardiner Keith R, Watson Peter R G

机构信息

Regional Regulatory Peptide Laboratory, Royal Hospitals Trust, Belfast, Northern Ireland, UK.

出版信息

Eur J Gastroenterol Hepatol. 2006 Feb;18(2):195-202. doi: 10.1097/00042737-200602000-00013.

Abstract

BACKGROUND

Coeliac disease is a common chronic inflammatory enteropathy characterized by villous atrophy and crypt hyperplasia in the small intestine. The mechanism of the intestinal damage in coeliac disease remains unclear. Glucagon-like peptide (GLP)-2 is an enterotrophic peptide that causes crypt hyperplasia and intestinal cell proliferation. We postulate that GLP-2 may be involved in the mucosal changes found in coeliac disease.

OBJECTIVES

To study plasma concentrations of GLP-2 in untreated patients with coeliac disease and determine the response to a gluten-free diet (GFD).

METHODS

A 440 kcal gluten-free test meal was given to seven controls and 12 coeliac patients at three time intervals: (1) before commencing a GFD; (2) 3 months after a GFD; and (3) 9 months after a GFD. Serial blood sampling was performed over a 2-h period. Each sample was analysed using radioimmunoassay for GLP-2, GLP-1, N-terminal glucagon (N-glucagon) and C-terminal glucagon (C-glucagon).

RESULTS

Untreated coeliac patients had significantly higher basal and peak GLP-2 and N-glucagon plasma concentrations compared with controls. After 3 months on a GFD, there was a significant decrease in basal GLP-2 plasma concentrations. There was no significant difference between GLP-1 or C-glucagon in untreated coeliac patients compared with controls.

CONCLUSION

This is the first reported study of GLP-2 in coeliac disease. After a GFD there is recovery of the intestine and a reduction in the GLP-2 trophic response. Our findings support the theory that GLP-2 may be part of the mucosal healing and maintenance mechanisms in coeliac disease.

摘要

背景

乳糜泻是一种常见的慢性炎症性肠病,其特征为小肠绒毛萎缩和隐窝增生。乳糜泻肠道损伤的机制尚不清楚。胰高血糖素样肽(GLP)-2是一种肠营养肽,可引起隐窝增生和肠细胞增殖。我们推测GLP-2可能参与了乳糜泻中发现的黏膜变化。

目的

研究未经治疗的乳糜泻患者血浆GLP-2浓度,并确定其对无麸质饮食(GFD)的反应。

方法

在三个时间点向7名对照者和12名乳糜泻患者给予440千卡的无麸质试验餐:(1)开始GFD之前;(2)GFD 3个月后;(3)GFD 9个月后。在2小时内进行系列采血。每个样本使用放射免疫分析法分析GLP-2、GLP-1、N端胰高血糖素(N-胰高血糖素)和C端胰高血糖素(C-胰高血糖素)。

结果

与对照者相比,未经治疗的乳糜泻患者基础和峰值GLP-2及N-胰高血糖素血浆浓度显著更高。GFD 3个月后,基础GLP-2血浆浓度显著降低。未经治疗的乳糜泻患者与对照者相比,GLP-1或C-胰高血糖素无显著差异。

结论

这是首次报道的关于乳糜泻中GLP-2的研究。GFD后肠道恢复,GLP-2营养反应降低。我们的研究结果支持GLP-2可能是乳糜泻黏膜愈合和维持机制一部分的理论。

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