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炎症性肠病中肠系膜脂肪组织中瘦素mRNA的过表达。

Overexpression of leptin mRNA in mesenteric adipose tissue in inflammatory bowel diseases.

作者信息

Barbier Maryse, Vidal Hubert, Desreumaux Pierre, Dubuquoy Laurent, Bourreille Arnaud, Colombel Jean-François, Cherbut Christine, Galmiche Jean-Paul

机构信息

Pôle Digestif et CIC-INSERM, CHU Nantes et INRA, 44093 Nantes Cedex 1.

出版信息

Gastroenterol Clin Biol. 2003 Nov;27(11):987-91.

PMID:14732844
Abstract

BACKGROUND

Leptin, a protein with a cytokine-like structure, is produced predominantly by adipocytes. It appears to play a key role in immune responses by increasing the secretion of Th1 and pro-inflammatory cytokines. As fat-wrapping is a characteristic feature of Crohn's disease (CD), and as increased leptin levels have been reported in animal models of intestinal inflammation, this study investigated whether mesenteric adipose tissue could be a source of leptin in human inflammatory bowel disease (IBD).

AIM

To quantify the expression of leptin mRNA in mesenteric adipose tissue of patients with CD or ulcerative colitis (UC).

METHODS

Specimens were obtained from mesenteric white adipose tissue close to healthy and inflammatory small intestine and/or colon in patients with CD or UC and, for controls, from apparently healthy mesentery of patients operated for carcinoma of the right colon. The expression of leptin mRNA was assessed by reverse transcription-competitive polymerase chain reaction.

RESULTS

Leptin mRNA levels were significantly higher in mesenteric adipose tissue of CD and UC patients than in controls (P<0.05). In CD and UC, concentrations were not significantly different in mesenteric fat specimens, whether contiguous to macroscopically normal or grossly abnormal intestine.

CONCLUSIONS

This study provides the first evidence of a novel abnormality of the mesentery of patients with IBD. Overexpression of leptin mRNA in mesenteric adipose tissue may contribute to (a) the inflammatory process, (b) enhancement of mesenteric TNF alpha expression in CD (as recently reported), and/or (c) the anorexia frequently reported during flares of IBD.

摘要

背景

瘦素是一种具有细胞因子样结构的蛋白质,主要由脂肪细胞产生。它似乎通过增加Th1和促炎细胞因子的分泌在免疫反应中起关键作用。由于脂肪包裹是克罗恩病(CD)的一个特征,并且在肠道炎症的动物模型中已报道瘦素水平升高,本研究调查了肠系膜脂肪组织是否可能是人类炎症性肠病(IBD)中瘦素的来源。

目的

量化CD或溃疡性结肠炎(UC)患者肠系膜脂肪组织中瘦素mRNA的表达。

方法

从CD或UC患者靠近健康和炎症性小肠及/或结肠的肠系膜白色脂肪组织中获取标本,作为对照,从因右结肠癌接受手术的患者看似健康的肠系膜中获取标本。通过逆转录竞争聚合酶链反应评估瘦素mRNA的表达。

结果

CD和UC患者肠系膜脂肪组织中的瘦素mRNA水平显著高于对照组(P<0.05)。在CD和UC中,无论肠系膜脂肪标本与宏观上正常或严重异常的肠道相邻,其浓度均无显著差异。

结论

本研究首次提供了IBD患者肠系膜新异常的证据。肠系膜脂肪组织中瘦素mRNA的过表达可能导致(a)炎症过程,(b)CD中肠系膜TNFα表达的增强(如最近报道),和/或(c)IBD发作期间频繁报道的厌食症。

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