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PNAS:年轻时的生活习惯或增加个体患乳腺癌的风险

来源:生物谷 2012-09-18 22:25

2012年9月18日 讯 /生物谷BIOON/ --近日,刊登在国际著名杂志PNAS上的一篇研究报告中,来自加州大学戴维斯分校的研究者指出,年轻时的生活习惯和其它相关因子或增加个体患乳腺癌的风险,而且这并不依赖于雌性激素的产量。这项研究或为调节正常乳腺发育或者乳腺癌的预防提供一些思路。

这项研究中,研究者以在饮食中添加10,12-共轭亚油酸为食的小鼠作为研究对象,这类似于模仿一种代谢综合征,人类中,这种代谢综合征和一系列的和肥胖相关的改变有关。小鼠饮食中添加10,12-共轭亚油酸因为其可以干扰正常的代谢过程,这项研究中,10,12-共轭亚油酸的补充可以刺激小鼠输乳管的生长,尽管小鼠缺少雌激素,添加10,12-共轭亚油酸后依然可以导致其输乳管的生长发育。

研究者指出,饮食诱导的乳腺发育同样可以增加某些小鼠乳房肿瘤的形成;同时研究者发现不同类型的小鼠对对不同的饮食添加物反应不同,尽管这些饮食添加物都会导致小鼠机体代谢的改变。这就表明,或许有一种遗传组分可以使得饮食和相关的代谢改变影响不同类型小鼠患乳腺癌的风险。

研究者Hovey表示,我们的研究发现或许为更好地理解年轻时饮食结构、代谢综合征和乳腺癌发展的关系。(生物谷Bioon.com)

编译自:Breast cancer risk linked to early-life diet and metabolic syndrome

Diet-induced metabolic change induces estrogen-independent allometric mammary growth

Grace E. Berryhilla, Julia M. Gloviczkia, Josephine F. Trotta, Lucila Aimoa, Jana Kraftb, Robert D. Cardiffc, Carly T. Paula, Whitney K. Petriea, Adam L. Lockd, and Russell C. Hoveya,1

Lifetime breast cancer risk reflects an unresolved combination of early life factors including diet, body mass index, metabolic syndrome, obesity, and age at first menses. In parallel, the onset of allometric growth by the mammary glands around puberty is widely held to be estrogen (E)-dependent. Here we report that several physiological changes associated with metabolic syndrome in response to a diet supplemented with the trans-10, cis-12 isomer of conjugated linoleic acid lead to ovary-independent allometric growth of the mammary ducts. The E-independence of this diet-induced growth was highlighted by the fact that it occurred both in male mice and with pharmacological inhibition of either E receptor function or E biosynthesis. Reversal of the metabolic phenotype with the peroxisome proliferator-activated receptor-γ agonist rosiglitazone abrogated diet-induced mammary growth. A role for hyperinsulinemia and increased insulin-like growth factor-I receptor (IGF-IR) expression during mammary growth induced by the trans-10, cis-12 isomer of conjugated linoleic acid was confirmed by its reversal upon pharmacological inhibition of IGF-IR function. Diet-stimulated ductal growth also increased mammary tumorigenesis in ovariectomized polyomavirus middle T-antigen mice. Our data demonstrate that diet-induced metabolic dysregulation, independently of ovarian function, stimulates allometric growth within the mammary glands via an IGF-IR-dependent mechanism.

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