Background: Obesity is associated with increased risks of Barrett’s oesophagus and oesophageal adenocarcinoma. Alterations in serum leptin and adiponectin, obesity-related cytokines, have been linked with several cancers and have been postulated as potential mediators of obesity-related carcinogenesis; however, the relationship with Barrett’s oesophagus remains unexplored.
Methods: Serum leptin and adiponectin concentrations were measured on two subsets of participants within a case–control study conducted in Brisbane, Australia. Cases were people aged 18–79 years with histologically confirmed Barrett’s oesophagus newly diagnosed between 2003 and 2006. Population controls, frequency matched by age and sex to cases, were randomly selected from the electoral roll. Phenotype and medical history data were collected through structured, self-completed questionnaires. Odds ratios (OR) and 95% CI were calculated using multivariable logistic regression analysis.
Results: In the pilot analysis (51 cases, 67 controls) risks of Barrett’s oesophagus were highest among those in the highest quartile of serum leptin (OR 4.6, 95% CI 0.6 to 33.4). No association was seen with adiponectin. In the leptin validation study (306 cases, 309 controls), there was a significant threefold increased risk of Barrett’s oesophagus among men in the highest quartile of serum leptin (OR 3.3, 95% CI 1.7 to 6.6) and this persisted after further adjustment for symptoms of gastro-oesophageal reflux (OR 2.4, 95% CI 1.1 to 5.2). In contrast, the risk of Barrett’s oesophagus among women decreased with increasing serum leptin concentrations.
Conclusions: High serum leptin is associated with an increased risk of Barrett’s oesophagus among men but not women. This association is not explained simply by higher body mass or gastro-oesophageal reflux among cases. The mechanism remains to be determined.
Statistics from Altmetric.com
Funding: This research was supported by grant number CA 001833-03 from the United States National Cancer Institute. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Cancer Institute. PMW and DCW are Senior Research Fellows of the National Health and Medical Research Council of Australia. NP is supported by a PhD scholarship from the National Health and Medical Research Council of Australia. The funding bodies played no role in the design or conduct of the study, the collection, management, analysis, or interpretation of the data, or the preparation, review or approval of the manuscript.
Ethics approval: Ethics approval was obtained.