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将身体活动与癌症风险及进展联系起来的生理和分子机制

[Physiologic and molecular mechanisms linking physical activity to cancer risk and progression].

作者信息

Ulrich C M, Wiskemann J, Steindorf K

机构信息

Abteilung Präventive Onkologie, Deutsches Krebsforschungszentrum und Nationales Centrum für Tumorerkrankungen, Heidelberg, Deutschland.

出版信息

Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2012 Jan;55(1):3-9. doi: 10.1007/s00103-011-1400-4.

DOI:10.1007/s00103-011-1400-4
PMID:22286244
Abstract

Physical activity is associated with a reduced risk of colon, breast, endometrial, lung, and pancreatic cancer. Evidence for mediating molecular mechanisms from experimental studies substantially strengthens the causal inference for this relationship. Randomized controlled trials indicate that exercise affects metabolic profiles, including hormone levels (estrogen, insulin signaling), inflammation (e.g., C-reactive protein), and adipokine concentrations (e.g., leptin). The size of the effect depends frequently on concurrent changes in body composition. There is also initial evidence for effects on immune function, oxidative stress, and possibly DNA repair capacity. Finally, outdoor physical activity can directly increase 25(OH)-vitamin D levels, providing another potential mechanism for linking physical activity to cancer risk. Randomized controlled studies with biomarker measurements are essential to increase evidence for causality and to identify the most effective intervention strategies and pharmacologic targets.

摘要

身体活动与降低患结肠癌、乳腺癌、子宫内膜癌、肺癌和胰腺癌的风险相关。来自实验研究的介导分子机制的证据大大加强了这种关系的因果推断。随机对照试验表明,运动影响代谢谱,包括激素水平(雌激素、胰岛素信号)、炎症(如C反应蛋白)和脂肪因子浓度(如瘦素)。效应的大小通常取决于身体成分的同时变化。也有初步证据表明运动对免疫功能、氧化应激以及可能的DNA修复能力有影响。最后,户外身体活动可直接提高25(OH)-维生素D水平,这为将身体活动与癌症风险联系起来提供了另一种潜在机制。进行有生物标志物测量的随机对照研究对于增加因果关系的证据以及确定最有效的干预策略和药物靶点至关重要。

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