Hsing Ann W, Sakoda Lori C, Chua Streamson
Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20852-7234, USA.
Am J Clin Nutr. 2007 Sep;86(3):s843-57. doi: 10.1093/ajcn/86.3.843S.
Although obesity has been consistently linked to an increased risk of several malignancies, including cancers of the colon, gallbladder, kidney, and pancreas, its role in prostate cancer etiology remains elusive. Data on the association between obesity and prostate cancer incidence are inconsistent, and in some studies obesity is associated with an increase in risk of high-grade prostate cancer but with a decrease in risk of low-grade tumors. In contrast, obesity has been consistently associated with an increased risk of prostate cancer aggressiveness and mortality. The differential effects of obesity on subtypes of prostate cancer suggest etiologic heterogeneity in these tumors and complex interactions between androgen metabolism and several putative risk factors, including insulin resistance, diabetes, inflammation, and genetic susceptibility, on prostate cancer risk. Data on the role of abdominal obesity, insulin resistance, and metabolic syndrome in prostate cancer etiology are limited. Obesity has been shown to be associated with a state of low-grade chronic inflammation, and insulin resistance and the metabolic syndrome are associated with adverse metabolic profiles and with higher circulating concentrations of inflammation-related markers, including leptin, interleukin-6, and tumor necrosis factor-, many of which have been shown to enhance tumor growth. Thus, whether obesity and metabolic syndrome modulate the risk of prostate cancer through chronic inflammation needs to be investigated further. Given that the prevalence of obesity and metabolic syndrome is increasing worldwide and that the world population is aging, the roles of obesity and metabolic syndrome in prostate carcinogenesis warrant further clarification.
尽管肥胖一直被认为与包括结肠癌、胆囊癌、肾癌和胰腺癌在内的多种恶性肿瘤风险增加有关，但其在前列腺癌病因学中的作用仍不明确。关于肥胖与前列腺癌发病率之间关联的数据并不一致，在一些研究中，肥胖与高级别前列腺癌风险增加相关，但与低级别肿瘤风险降低相关。相比之下，肥胖一直与前列腺癌侵袭性和死亡率风险增加相关。肥胖对前列腺癌亚型的不同影响表明这些肿瘤存在病因异质性，以及雄激素代谢与包括胰岛素抵抗、糖尿病、炎症和遗传易感性在内的几种假定风险因素之间在前列腺癌风险方面存在复杂的相互作用。关于腹部肥胖、胰岛素抵抗和代谢综合征在前列腺癌病因学中的作用的数据有限。肥胖已被证明与低度慢性炎症状态相关，胰岛素抵抗和代谢综合征与不良代谢特征以及包括瘦素、白细胞介素 - 6 和肿瘤坏死因子 - 在内的炎症相关标志物的循环浓度升高相关，其中许多已被证明可促进肿瘤生长。因此，肥胖和代谢综合征是否通过慢性炎症调节前列腺癌风险需要进一步研究。鉴于肥胖和代谢综合征在全球范围内的患病率正在上升，且世界人口正在老龄化，肥胖和代谢综合征在前列腺癌发生中的作用值得进一步阐明。
