Obesity and Carcinogenesis
摘要
Obesity is reaching epidemic levels worldwide, a troubling phenomenon that increases the risk of cardiovascular diseases and type 2 diabetes. Recently, it has been suggested that obesity has a pathological link with cancer. Obesity is strongly associated with changes in the physiological function of adipose tissue, leading to insulin resistance, chronic inflammation, and altered secretion of adipokines. Several of these factors are directly involved in carcinogenesis and cancer progression, such as insulin resistance, increased levels of leptin, plasminogen activator inhibitor-1, endogenous sex steroids, decreased levels of adiponectin, and chronic inflammation. Additionally, adipose tissue has also been hypothesized to act as a reservoir for lipophilic, liposoluble environmental carcinogens, so that chemical pollution may indirectly promote both overweight/obesity and cancer. Moreover, it has also been suggested that many carcinogens stored in the adipose tissue could be released in periodic doses in the circulatory system and therefore target peripheral tissues to induce carcinogenesis. Such carcinogens mainly include organochlorine pesticides and polychlorinated biphenyls (PCBs). Their association with an increased risk of cancer appears to have been demonstrated for breast and prostate carcinoma, as well as for lymphoma. In this study, we reviewed the relevant evidence focusing on adipose tissue dysfunction as a unifying causal factor for cancer, as well as the hypothesis of chemical pollutants and their link to obesity and carcinogenesis.