The association of gastric leptin with oesophageal inflammation and metaplasia
The association of gastric leptin with oesophageal inflammation and metaplasia
复制标题
DOI：
10.1136/gut.2007.131672
复制
发表时间：
2008-01-01
期刊：
影响因子：
24.5
通讯作者：
Blaser, M. J.
中科院分区：
文献类型：
--
作者：
Francois, F.;Roper, J.;Blaser, M. J.
背景：胃食管反流病并发症可能反映了保护性因素和损害性因素之间的失衡。通过其对细胞生长的影响，瘦素可能会影响食管粘膜homeostasis.Aims：要确定是否瘦素受体存在于食管，以及是否血清或胃瘦素水平与食管炎症和化生。方法：从患者提到的上消化道内窥镜检查，从胃和远端食管活检，并收集血清样本。患者分为正常、发炎或Barrett食管。定量免疫组化进行了代表性的部分，血浆和胃活检标本中的瘦素水平测定特异性immunoassociation.Results：269人参加，105幽门螺杆菌阴性。在88例完整食管活检的患者中，44例正常，24例炎症，20例Barrett食管。瘦素受体在食管上皮细胞上高度表达，在所有三种情况下具有相似的密度和染色模式，血浆和胃窦瘦素水平没有显着差异。与正常（126（78-221）pg/ mg）或炎症（114（76-195）pg/mg）食管相比，Barrett's患者的胃底瘦素水平（中位数202（四分位数间距123-333）pg/ mg）显著（p = 0.01）较高。在多变量分析中，每增加一倍的胃底瘦素，有巴雷特的几率是3.4倍（95%CI 1.5至7.6）高相比，有一个正常的oesophageal.Conclusions：瘦素受体表达食管上皮细胞提供了一个途径，瘦素介导的信号转导。胃瘦素产生的变化可能有助于差异食管愈合和化生进展。
Background: Gastro-oesophageal reflux disease complications may reflect imbalances between protective and injurious factors. Through its effects on cell growth, leptin may influence oesophageal mucosal homeostasis.Aims: To determine whether leptin receptors are present in the oesophagus, and whether serum or gastric leptin levels are associated with oesophageal inflammation and metaplasia.Methods: From patients referred for upper endoscopy, biopsies were obtained from the stomach and distal oesophagus, and serum samples were collected. Patients were classified as having normal, inflamed or Barrett's oesophagus. Quantitative immunohistochemistry was performed on representative sections, and leptin levels in plasma and gastric biopsy samples were determined by specific immunoassay.Results: Of 269 individuals enrolled, 105 were Helicobacter pylori-negative. Of the 88 patients with complete oesophageal biopsies, 44 were normal, 24 were inflamed and 20 were Barrett's oesophagus. Receptors for leptin were highly expressed on oesophageal epithelial cells, with similar density and staining pattern in all three conditions, and plasma and antral leptin levels did not differ significantly. Patients with Barrett's had significantly (p = 0.01) higher fundic leptin levels (median 202 (interquartile range 123-333) pg/ mg) compared with normal (126 (78-221) pg/ mg) or inflamed (114 (76-195) pg/ mg) oesophagus. In multivariate analysis, for every twofold increase in fundic leptin, the odds of having Barrett's was 3.4 times (95% CI 1.5 to 7.6) higher compared with having a normal oesophagus.Conclusions: Leptin receptor expression on oesophageal epithelial cells provides a pathway for leptin-mediated signal transduction. Variation in gastric leptin production could contribute to differential oesophageal healing and metaplasia progression.