Serum Leptin and Adiponectin Levels and Risk of Barrett’s Esophagus and Intestinal Metaplasia of the Gastroesophageal Junction.
 Nutritional Sciences Program, The University of Washington, Seattle, Washington, USA  Division of Public Health Sciences, The Fred Hutchinson Cancer Research Center, Seattle, Washington, USA  The Center for Human Nutrition, Omaha, Nebraska, USA  Department of Health Promotion, Social & Behavioral Health, College of Public Health, The University of Nebraska Medical Center, Omaha, Nebraska, USA.
Persons diagnosed with Barrett’s esophagus (BE) are at increased risk of developing esophageal adenocarcinoma (EA). Obesity is a major risk factor for both BE and EA. The primary purposes of this study were to determine whether circulating levels of leptin and adiponectin, both of which are deregulated in obese states, predict risk of specialized intestinal metaplasia (SIM) occurring in the esophagus (BE) and/or gastroesophageal junction, and evaluate the extent to which they mediate the relationship between obesity and these conditions. In this case-control study, 177 persons newly diagnosed with SIM were compared with 173 general population controls using unconditional logistic regression. Females in the highest tertiles of BMI and waist circumference were at the greatest risk (adjusted odds ratio (OR) = 4.6 (95% confidence interval (CI) = 1.9, 11.6), P(trend) = 0.002; OR = 5.1 (95% CI = 2.0, 13.0), P(trend) = 0.002, respectively) compared to females in the lowest tertiles. Adjustment for leptin and adiponectin attenuated these associations by 52 and 42%, respectively. Males in the highest tertile of waist-to-hip ratio were at the greatest risk (adjusted OR = 2.8 (95% CI = 1.3, 5.9), P(trend) = 0.014) compared to males in the lowest tertile. However, adjustment for leptin and adiponectin did not attenuate these associations. Our study results are consistent with the notion that circulating leptin and adiponectin partially mediate the obesity-BE relationship in women. Leptin and adiponectin’s role in the progression from normal epithelium to SIM/BE and on to EA should be further elucidated.
PMID: 20111023 [PubMed – as supplied by publisher]