Circulating adipokines and risk of obesity related cancers: A systematic review and meta-analysis

Abstract

BackgroundObesity can influence on carcinogenesis through alterations in adipokines and subsequent inflammatory changes. This meta-analysis was aimed to comprehensively assess the association between circulating adipokines and risk of obesity-related cancers. MethodsPubmed and Embase were searched up to October 2017 for observational studies investigating the relationship between adipokines and cancers. Pooled odds ratio and the corresponding 95% confidence interval was estimated through the meta-analysis using a random-effects model.Findings A total of 93 observational studies (adiponectin = 60, high molecular weight adiponectin = 9, leptin = 39, IL-6 = 16, TNF-α = 10, and resistin = 17) were included. Adiponectin was significantly associated with decreased risk of cancer (pooled OR 0.70, 95% CI 0.60–0.80; I2 = 71.9%; Pheterogeneity <0.01). Leptin was significantly associated with increased risk of cancer (1.26, 1.05–1.51; I2 = 65.7%; Pheterogeneity <0.01). For each 5 μg/ml increase in adiponectin and 5 ng/ml increase in leptin, the pooled OR was 0.88 (0.83–0.93; I2 = 80.2%; Pheterogeneity <0.01) and 1.05 (1.01–1.09; I2 = 67.9%; Pheterogeneity<0.01)), respectively. There was nonlinear dose-response association (Pnonlinearity for adiponectin = 0.01; Pnonlinearity for leptin = 0.003).IL-6 (1.09, 0.94–1.25), TNF- α (1.65, 0.99–2.74), and resistin (1.28, 0.78–2.11) was not associated with risk of cancer. By cancer site and type, highest category of adiponectin was associated with decreased risk of breast (OR 0.74, 0.60-0.91), colorectal (0.74, 0.60–0.91), and endometrial cancer (0.49, 0.34–0.72). Higher leptin was associated with increased risk of endometrial (1.88, 1.24–2.87) and kidney cancer (2.07, 1.51–2.83). ConclusionOur study suggests that adiponectin and leptin may play a role in the etiology of cancer.