BACKGROUND AND AIMS: Gastroesophageal reflux disease (GERD) and obesity are associated with esophageal adenocarcinoma (EAC). We hypothesized that the obesity-EAC relation is mediated by factors secreted from adipocytes. Adiponectin is a peptide secreted by adipocytes, and its plasma levels are inversely associated with obesity. We aimed to estimate the effect of circulating adiponectin on the risk of Barrett's esophagus (BE), an accepted precursor of EAC, controlling for GERD symptoms and other potential confounders. METHODS: We conducted a case-control study in cases of BE compared with controls without BE; most controls had GERD. Odds ratios (OR), corresponding to associations with BE, were estimated from conditional and unconditional logistic regression analyses of 50 matched pairs. RESULTS: BE was inversely associated with plasma adiponectin level (OR for each 10-microg/mL decrement 4.7, 95% confidence interval [CI] 1.4-15.0) and positively associated with GERD duration >or=10 yr, male gender, tobacco smoking, body mass index (BMI), waist circumference, and waist-to-hip ratio. Further adjustment for GERD duration, tobacco use, and BMI increased the adiponectin-BE association (OR 6.4, 95% CI 1.1-37.0), but the estimated OR was reduced when adjusting for measures of abdominal obesity (e.g., OR 2.5, 95% CI 0.49-13.00) and further adjusting for gender (OR 1.8, 95% CI 0.66-4.70). CONCLUSIONS: Despite methodologic limitations, including the small sample size, our findings suggest that adiponectin may be involved in the etiology of BE. Rather than simply a mechanical effect of obesity promoting GERD, the effects of abdominal obesity on the risk of BE might be mediated by adiponectin and other circulating factors.
BACKGROUND AND AIMS: Gastroesophageal reflux disease (GERD) and obesity are associated with esophageal adenocarcinoma (EAC). We hypothesized that the obesity-EAC relation is mediated by factors secreted from adipocytes. Adiponectin is a peptide secreted by adipocytes, and its plasma levels are inversely associated with obesity. We aimed to estimate the effect of circulating adiponectin on the risk of Barrett's esophagus (BE), an accepted precursor of EAC, controlling for GERD symptoms and other potential confounders. METHODS: We conducted a case-control study in cases of BE compared with controls without BE; most controls had GERD. Odds ratios (OR), corresponding to associations with BE, were estimated from conditional and unconditional logistic regression analyses of 50 matched pairs. RESULTS: BE was inversely associated with plasma adiponectin level (OR for each 10-microg/mL decrement 4.7, 95% confidence interval [CI] 1.4-15.0) and positively associated with GERD duration >or=10 yr, male gender, tobacco smoking, body mass index (BMI), waist circumference, and waist-to-hip ratio. Further adjustment for GERD duration, tobacco use, and BMI increased the adiponectin-BE association (OR 6.4, 95% CI 1.1-37.0), but the estimated OR was reduced when adjusting for measures of abdominal obesity (e.g., OR 2.5, 95% CI 0.49-13.00) and further adjusting for gender (OR 1.8, 95% CI 0.66-4.70). CONCLUSIONS: Despite methodologic limitations, including the small sample size, our findings suggest that adiponectin may be involved in the etiology of BE. Rather than simply a mechanical effect of obesity promoting GERD, the effects of abdominal obesity on the risk of BE might be mediated by adiponectin and other circulating factors.
Authors: Siddharth Singh; Anamay N Sharma; Mohammad Hassan Murad; Navtej S Buttar; Hashem B El-Serag; David A Katzka; Prasad G Iyer Journal: Clin Gastroenterol Hepatol Date: 2013-05-22 Impact factor: 11.382
Authors: Jose M Garcia; Andres E Splenser; Jennifer Kramer; Abeer Alsarraj; Stephanie Fitzgerald; David Ramsey; Hashem B El-Serag Journal: Clin Gastroenterol Hepatol Date: 2013-08-15 Impact factor: 11.382
Authors: Stuart Jon Spechler; Rebecca C Fitzgerald; Ganapathy A Prasad; Kenneth K Wang Journal: Gastroenterology Date: 2010-01-18 Impact factor: 22.682