{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T17:12:04Z","timestamp":1776964324030,"version":"3.51.4"},"reference-count":69,"publisher":"BMJ","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aims:<\/jats:title>\n                    <jats:p>To determine whether leptin receptors are present in the oesophagus, and whether serum or gastric leptin levels are associated with oesophageal inflammation and metaplasia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>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\u2019s oesophagus. Quantitative immunohistochemistry was performed on representative sections, and leptin levels in plasma and gastric biopsy samples were determined by specific immunoassay.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Of 269 individuals enrolled, 105 were\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      -negative. Of the 88 patients with complete oesophageal biopsies, 44 were normal, 24 were inflamed and 20 were Barrett\u2019s 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\u2019s had significantly (p\u200a=\u200a0.01) higher fundic leptin levels (median 202 (interquartile range 123\u2013333) pg\/mg) compared with normal (126 (78\u2013221) pg\/mg) or inflamed (114 (76\u2013195) pg\/mg) oesophagus. In multivariate analysis, for every twofold increase in fundic leptin, the odds of having Barrett\u2019s was 3.4 times (95% CI 1.5 to 7.6) higher compared with having a normal oesophagus.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/gut.2007.131672","type":"journal-article","created":{"date-parts":[[2007,8,30]],"date-time":"2007-08-30T20:53:41Z","timestamp":1188507221000},"page":"16-24","source":"Crossref","is-referenced-by-count":66,"title":["The association of gastric leptin with oesophageal inflammation and metaplasia"],"prefix":"10.1136","volume":"57","author":[{"given":"F","family":"Francois","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J","family":"Roper","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A J","family":"Goodman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Z","family":"Pei","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Ghumman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Mourad","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A Z Olivares","family":"de Perez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G I","family":"Perez-Perez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C-H","family":"Tseng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M J","family":"Blaser","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[2007,8,30]]},"reference":[{"key":"2025112111020435000_57.1.16.1","doi-asserted-by":"crossref","first-page":"11","DOI":"10.1111\/j.1365-2036.2005.02605.x","article-title":"Review article: gastro-oesophageal reflux disease\u2014the extent of the problem.","volume":"22","author":"Moayyedi","year":"2005","journal-title":"Aliment Pharmacol Ther"},{"key":"2025112111020435000_57.1.16.2","doi-asserted-by":"publisher","DOI":"10.1053\/gast.1996.v111.pm8898632"},{"key":"2025112111020435000_57.1.16.3","doi-asserted-by":"crossref","first-page":"1149","DOI":"10.1016\/0016-5085(91)90062-P","article-title":"A critical analysis, with appropriate controls, of gastric acid and pepsin secretion in clinical esophagitis.","volume":"101","author":"Hirschowitz","year":"1991","journal-title":"Gastroenterology"},{"key":"2025112111020435000_57.1.16.4","first-page":"1293","article-title":"Risk factors for Barrett\u2019s esophagus in community-based practice. 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