Numerous studies have investigated the association between obesity and prostate cancer (CaP), although the results have not been concluding due to the great difficulty to evaluate the effects of obesity on the development of this type of tumor. The aim of this study was to carry out a comprehensive over-view of the existing evidence about the role of adipose tissue in the prostate carcinogenesis. Recent evidence suggests that androgens, leptin, IL-6, VEGF, insulin and IGF-1 may play a role in PC progression, while adiponectin and IGFBP-3 may act as "anti-prostatic cancer" adipokines. The potential mechanisms by which obesity may initiate, promote or facilitate the progression of CaP are low levels of testosterone and high levels of estrogen, coexisting metabolic syndrome, increased secretion of leptin, VEGF, IL-6 and TNF-alpha and decreased adiponectin, and excessive intake of saturated fat.
Conclusion: Obesity may promote the progression of established PC rather than being a risk factor for the development of this tumour. However, additional studies are needed to clarify the relationship between adipokines and PC before developing new preventive or treatment strategies for this tumor.