脂肪细胞或在抗乳腺癌中起关键作用
既往研究显示，肥胖与乳腺癌相关，其分子机制受到白脂肪组织分泌的激脂激素调控，脂连蛋白和瘦蛋白可能是肥胖者死亡风险较高以及效果不佳的原因。
2016年7月1日，美国生理学会官方期刊《应用生理学杂志》正式发表加拿大约克大学的研究报告，发现脂肪细胞可通过最有效的方式（如运动等锻炼方式）对抗乳腺癌。
该研究使用啮齿动物模型，观察脂肪细胞是否对肥胖和乳腺癌之间的相关性起作用，以及针对肥胖的干预措施能否消除乳腺癌风险。
结果发现，肥胖者体内脂肪细胞产生的激素可促进乳腺癌生长，而消瘦者体内脂肪细胞产生的激素会阻止乳腺癌生长。这些激素的特点取决于人们是瘦还是胖，并且胖和瘦决定了癌症是否生长。
研究表明，自愿和严格的锻炼可消除甚至可完全避免由肥胖引起的肿瘤生长，即使适度运动也可导致乳腺癌增长放缓，只要进行更多锻炼，好处就越大。
因此，锻炼是几乎没有不良副作用的抗癌药物，锻炼对某些乳腺癌患者而言可能成为一种方法。
J Appl Physiol. 2016 Jul 1;121(1):139-53.
Voluntary physical activity abolishes the proliferative tumor growth microenvironment created by adipose tissue in animals fed a high fat diet.
Theriau CF, Shpilberg Y, Riddell MC, Connor MK.
proliferation
York University, Toronto, Ontario, Canada.
The molecular mechanisms behind the obesity-breast cancer association may be regulated via adipokine secretion by white adipose tissue. Specifically, adiponectin and leptin are altered with adiposity and exert antagonistic effects on cancer cell proliferation. We set out to determine whether altering adiposity in vivo via high fat diet (HFD) feeding changed the tumor growth supporting nature of adipose tissue and whether voluntary physical activity (PA) could ameliorate these HFD-dependent effects. We show that condit
ioned media (CM) created from the adipose tissue of HFD fed animals caused an increase in the proliferation of MCF7 cells compared with cells exposed to CM prepared from the adipose of lean chow diet fed counterparts. This increased proliferation was driven within the MCF7 cells by an HFD-dependent antagonism between AMP-activated protein kinase (AMPK) and protein kinase B (Akt) signaling pathways, decreasing p27 protein levels via reduced phosphorylation at T198 and downregulation of adiponectin receptor 1 (AdipoR1). PA can ameliorate these proliferative effects of HFD-CM on MCF7 cells, increasing p27(T198) by AMPK, reducing pAkt(T308), and increasing AdipoR1, resulting in cell cycle withdrawal in a manner that depends on the PA intensity. High physical activity (>3 km/day) completely abolished the effects of HFD feeding. In addition, AdipoR1 overexpression mimics the effects of exercise, abolishing the proliferative effects of the HFD-CM on MCF7 cells and further enhancing the antiproliferative effects of PA on the HFD-CM. Thus voluntary PA represents a means to counteract the proliferative effects of adipose tissue on breast cancers in obese patients.

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