Obesity and Prostate Cancer: A Role for Adipokines

ObjectivesMany studies have investigated the association between obesity and prostate cancer risk but have yielded inconsistent results. Recent evidence suggests a particular role for obesity in prostate cancer progression. Many studies have investigated the roles of adipose tissue-derived factors (adipokines) as putative molecular mediators between obesity and prostate cancer. This review provides an overview of current evidence that supports such a role for adipokines.MethodsA comprehensive literature review was carried out using PubMed to search for articles relating to prostate cancer and the following adipokines: leptin, interleukin 6, vascular endothelial growth factor (VEGF), and adiponectin.ResultsProstate cancer cells are exposed to adipokines either via the circulation or through locally produced adipokines following invasion of the retropubic fat pad. Circulating levels of most adipokines are positively correlated with obesity; adiponectin is inversely correlated with obesity. High circulating levels of leptin, interleukin 6, and VEGF are associated with increased prostate cancer risk and increased aggressiveness. Adiponectin levels are lower in patients with prostate cancer and are inversely associated with grade of disease. Adipokines exert a variety of biologic effects on prostate cancer cells, modulating cellular differentiation, apoptosis, proliferation, and angiogenesis.ConclusionsEvidence suggests a role for obesity and adipokines in promoting the progression of established prostate cancer. Adipokines may contribute to the molecular basis for the association between obesity and prostate cancer, but the complex pathophysiology of both these disease states requires further studies.