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代谢失衡与前列腺癌进展

Metabolic imbalance and prostate cancer progression.

作者信息

Burton Anya J, Tilling Kate M, Holly Jeff M, Hamdy Freddie C, Rowlands Mari-Anne E, Donovan Jenny L, Martin Richard M

出版信息

Int J Mol Epidemiol Genet. 2010 Jul 25;1(4):248-71.

Abstract

There is substantial evidence implicating environmental factors in the progression of prostate cancer. The metabolic consequences of a western lifestyle, such as obesity, insulin resistance and abnormal hormone production have been linked to prostate carcinogenesis through multiple overlapping pathways. Insulin resistance results in raised levels of the mitogens insulin and insulin-like growth factor-1, both of which may affect prostate cancer directly, or through their effect on other metabolic regulators. Obesity is associated with abnormal levels of adipocyte-derived peptides (adipokines), sex hormones and inflammatory cytokines. Adipokines have been shown to influence prostate cancer in both cell culture studies and observational, population level studies. Testosterone appears to have a complex relationship with prostate carcinogenesis, and it has been suggested that the lower levels associated with obesity may select for more aggressive androgen independent prostate cancer cells. Prostatic inflammation, caused by infection, urinary reflux or dietary toxins, frequently occurs prior to cancer development and may influence progression to advanced disease. High levels of ω-6 fatty acids in the diet may lead to the production of further inflammatory molecules that may influence prostate cancer. Increased fatty acid metabolism occurs within tumour cells, providing a potential target for prostate cancer therapies. Aberrations in amino acid metabolism have also been identified in prostate cancer tissue, particularly in metastatic cancer. This evidence indicates lifestyle interventions may be effective in reducing the incidence of clinical disease. However, much more research is needed before recommendations are made.

摘要

有大量证据表明环境因素与前列腺癌的进展有关。西方生活方式的代谢后果,如肥胖、胰岛素抵抗和激素分泌异常,已通过多种重叠途径与前列腺癌发生相关联。胰岛素抵抗导致有丝分裂原胰岛素和胰岛素样生长因子-1水平升高,这两者可能直接影响前列腺癌,或通过它们对其他代谢调节因子的作用来影响。肥胖与脂肪细胞衍生肽(脂肪因子)、性激素和炎性细胞因子水平异常有关。在细胞培养研究以及观察性人群水平研究中均已表明脂肪因子会影响前列腺癌。睾酮与前列腺癌发生似乎存在复杂关系,有人提出与肥胖相关的较低睾酮水平可能会选择出更具侵袭性的雄激素非依赖性前列腺癌细胞。由感染、尿液反流或饮食毒素引起的前列腺炎症在癌症发展之前经常发生,并且可能影响疾病进展至晚期。饮食中高水平的ω-6脂肪酸可能导致产生更多可能影响前列腺癌的炎症分子。肿瘤细胞内脂肪酸代谢增加,这为前列腺癌治疗提供了一个潜在靶点。在前列腺癌组织中,特别是在转移性癌症中,也发现了氨基酸代谢异常。这一证据表明生活方式干预可能有效降低临床疾病的发病率。然而,在提出建议之前还需要进行更多研究

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