title: The association of gastric leptin with oesophageal inflammation and metaplasia.
abstract: 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.
  
  
  OBJECTIVE
  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.
authors.affiliation: New York University School of Medicine, New York, NY, USA. fritz.francois@med.nyu.edu
authors.forename: F
authors.initials: F
authors.lastname: Francois
authors.forename: J
authors.initials: J
authors.lastname: Roper
authors.forename: A J
authors.initials: AJ
authors.lastname: Goodman
authors.forename: Z
authors.initials: Z
authors.lastname: Pei
authors.forename: M
authors.initials: M
authors.lastname: Ghumman
authors.forename: M
authors.initials: M
authors.lastname: Mourad
authors.forename: A Z Olivares
authors.initials: AZ
authors.lastname: de Perez
authors.forename: G I
authors.initials: GI
authors.lastname: Perez-Perez
authors.forename: C-H
authors.initials: CH
authors.lastname: Tseng
authors.forename: M J
authors.initials: MJ
authors.lastname: Blaser
mesh_terms: D001471:Barrett Esophagus / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D016145:Endoscopy, Digestive System; D004941:Esophagitis / Q000378:metabolism* / Q000473:pathology; D004947:Esophagus / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D020738:Leptin / Q000378:metabolism*; D008297:Male; D008679:Metaplasia / Q000209:etiology / Q000378:metabolism; D008875:Middle Aged; D054411:Receptors, Leptin / Q000378:metabolism*; D012189:Retrospective Studies; D012680:Sensitivity and Specificity
chemical_list: D020738:Leptin; D054411:Receptors, Leptin