Abstract
Background. Obesity is now a well-established risk factor for colon neoplasia, yet the biological mechanisms underlying this link are not fully understood. Increasing data support that adipokines play an important role in colon carcinogenesis, and it is hypothesized that adipokines may in part mediate the link between obesity and colon neoplasia. To date, few epidemiological studies have explicitly examined this hypothesis.
Methods. We investigated whether adipokines mediate the obesity-colon adenoma association and whether mediating effects differ by race in a sample of Caucasians (217 cases and 650 controls) and African Americans (175 cases and 378 controls) participating in the Cleveland Colonoscopy Screening Study. We examined potential mediating effects of leptin and adiponectin by 1) regression analyses assessing whether leptin and adiponectin attenuate the association of waist-to-hip ratio and adenomatous polyps, and 2) path analysis assessing whether leptin or adiponectin are mediators of the obesity-adenomatous polyp association.
Results. Neither leptin nor adiponectin showed evidence for attenuation of the WHR-adenomatous polyp association, nor did we identify a statistically significant mediating effect of leptin or adiponectin via the Sobel method (all Sobel p>0.27).
Conclusion. Our study is unable to support mediating roles of leptin and adiponectin in association of obesity and colon adenoma. Larger studies on how these associations vary by race, sex, and obesity are needed, as well as studies that investigate whether adipokines have mediating effects in later stages of carcinogenesis.
Citation Format: Heather M. Ochs-Balcom, Rikki Cannioto, Zhengyi Chen, Cheryl Thompson, Jing Nie, Amy E. Millen, Jo L. Freudenheim, Russell Tracy, Li Li. Do adipokines mediate the association between obesity and adenomatous polyps?. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr B13. doi:10.1158/1538-7755.DISP13-B13