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The association of gastric leptin with esophageal inflammation and metaplasia
  1. Fritz Francois (fritz.francois{at}
  1. NYU School of Medicine, United States
    1. Jatin Roper (jatinroper{at}
    1. NYU School of Medicine, United States
      1. Adam Goodman (goodma02{at}
      1. NYU School of Medicine, United States
        1. Zhiheng Pei (zhiheng.pei{at}
        1. NYU School of Medicine, United States
          1. Muhammad Ghumman (msg278{at}
          1. NYU School of Medicine, United States
            1. Michelle Mourad (michellemourad{at}
            1. University of California San Francisco, United States
              1. Asalia Z. Olivares de Perez (olivaa01{at}
              1. NYU School of Medicine, United States
                1. Guillermo I. Perez-Perez (perezg02{at}
                1. NYU School of Medicine, United States
                  1. Chi-Hong Tseng (ch.tseng{at}
                  1. NYU School of Medicine, United States
                    1. Martin J. Blaser (martin.blaser{at}
                    1. NYU School of Medicine, United States


                      Background Gastroesophageal reflux disease (GERD) complications may reflect imbalances between protective and injurious factors. Through its effects on cell growth, leptin may influence esophageal mucosal homeostasis.

                      Aims To determine whether leptin receptors are present in the esophagus, and whether serum or gastric leptin levels are associated with esophageal inflammation and metaplasia.

                      Methods From patients referred for upper endoscopy, biopsies were obtained from the stomach and distal esophagus and serum samples were collected. Patients were classified as having normal, inflamed, or Barrett's esophagus. 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 H. pylori-negative. Of the 88 patients with complete esophageal biopsies, 44 were normal, 24 were inflamed, and 20 were Barrett's esophagus. Receptors for leptin were highly expressed on esophageal 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 pg/mg (IQR 123-333)] compared to normal [126 pg/mg (78-221)] or inflamed [114 pg/mg (76-195)] esophagus. In multivariate analysis, for every 2-fold increase in fundic leptin, the odds of having Barrett's was 3.4 times [95% CI 1.5-7.6] higher compared to having a normal esophagus.

                      Conclusions Leptin receptor expression on esophageal epithelial cells provides a pathway for leptin-mediated signal transduction. Variation in gastric leptin production could contribute to differential esophageal healing and metaplasia progression.

                      • Barrett esophagus
                      • Gastroesophageal reflux
                      • Inflammation
                      • Leptin
                      • Leptin receptor

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