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Sicience and technology
科学和技术
Cancer and obesity
癌症与肥胖
Malignant flab
恶性松弛
At last, an understanding of how overeating causes cancer
吃得过多如何导致癌症
OVERWEIGHT women are more likely to develop breast cancer than lean ones.
超重的女人相比偏瘦的女人更容易得乳癌。
Why has been a mystery.
原因一直以来都是个迷。
But it is now less mysterious thanks to the work of Kevin Gardner, a researcher at America's National Cancer Institute in Bethesda, Maryland.
但由于马里兰州美国国家癌症协会研究院KG研究员为此做出的努力，现在并没有之前那么神秘了。
Dr Gardner and his colleagues have found that processing calories affects the activity of BRCA1, a gene that encodes a well-known tumour-suppression protein.
KG博士和他的同事们发现合成卡路里的过程会影响BRCA1基因的活性，该基因为一种著名的抗肿瘤蛋白质编码。
Mutations of this gene are strong predictors of breast and ovarian cancer—so strong that the gene's DNA sequence is the subject of litigation in America about whether natural gene sequences can be patented, and thus the market in tests for these mutations cornered.
BRCA1基因的突变是乳癌和卵巢癌的强烈预报器---如此强烈以至于在美国，常常就有关自然基因序列是否可以申请专利这样的问题发生诉讼，因此测试这些突变的市场被垄断了。
Dr Gardner's discovery is that a substance called C-terminal binding protein helps regulate BRCA1.
KG博士发现了一种能够调节BRCA1基因的蛋白质CtBP。
Since the activity of CtBP is, itself, governed by the processing of calorie-rich molecules, the more of those molecules the body processes, the more at risk of cancer it becomes.
因为CtBP蛋白质本身由加工富含卡路里的分子的过程控制着，所以身体处理越多的这类分子，患癌症的风险就越大。
Previous work has shown that CtBP senses the amount of energy in a cell by binding to a small molecule called NADH.
之前的工作表明，CtBP蛋白质通过结合一种叫做NADH的小分子来感知每个细胞中的总能量。
This chemical is a by-product of metabolism, and cells that are processing an excessive amount of energy for storage have a superabundance of it compared with the amount of a related molecule called NAD+.
这种化学物质是新陈代谢的副产物，并且那些处理并存储过剩能量的细胞拥有过剩的NADH分子，
As the ratio of NAD+ to NADH falls, CtBP combines with NADH.
和与之有关叫做NAD+的分子比起来。
This changes CtBP's shape and enables it to form complexes with several other proteins.
这改变了CtBP的形状并使之形成一种带有其他蛋白质的联合体。
These complexes control the activity of DNA by shutting off certain genes.
这些联合体通过切断某些基因控制DNA活动。
Dr Gardner and his team report in the latest issue of Nature Structural & Molecular Biology that one of the genes so controlled is BRCA1.
KG博士和他的团队在最新一期的《自然结构和分子生物》上宣称，其中这么被控制的基因中就有BRCA1。
The protein encoded by BRCA1 is involved in DNA repair.
被BRCA1基因编码的蛋白质与DNA修复有关。
Cells that lack a working version of it gradually accumulate genetic changes.
缺乏它的一个工作版本的细胞们渐渐引起了基因的改变。
Though most of these changes either have little impact or will lead to the cell's death, some may promote the formation or progression of tumours.
尽管多数改变要么影响不大，要么会导致细胞死亡，但有些可能会刺激肿瘤的形成或恶化。
A low NAD+/NADH ratio, according to Dr Gardner's work, has a similar effect to a BRCA1 mutation.
据KG博士的研究工作，低水平的NAD+/NADH对BRCA1突变会产生类似作用。
It leads to less DNA repair and more mutations.
这导致了DNA修复的减少却增加了基因的突变的可能性。
That, unfortunately, combines with another effect of too much fat, which is that it stimulates the production of oestrogen by cells that are involved in the storage of fat.
不幸的是，这和另外一个过多摄入脂肪的影响就结合起来，过多摄入脂肪通过那些储存脂肪的细胞会刺激雌激素的产生。更多的雌激素意味着荷尔蒙细胞增殖—这是一种非常敏感的组织—包括乳房和卵巢。
More oestrogen means more cell proliferation in hormone-sensitive tissues—a category that includes the breasts and the ovaries. Therefore, just when those cells are being told to undergo the error-prone process of replication and division and need their DNA-repair system most, CtBP slashes that system to ribbons.
因此，当这些细胞被通知经历可能会出错的复制和分裂过程并需要他们的DNA修复系统时，CtBP就会将此系统破坏。
Though this is the first clear link between calorie intake and cancer that has been seen at the molecular level, Dr Gardner says his result is consistent with numerous past experiments.
尽管这是摄入热量和癌症之间联系的首次清晰描述，该联系是在分子水平下被发现的，但KG博士说，他的研究结果与之前的大量实验一致。
For example, breast tumours are more aggressive and less genetically stable in heavily fed mice than in animals confined to a calorie-restricted diet.
例如，与那些吃热量受限制食物的老鼠相比，不加限制的老鼠的乳房肿块更恶性且基因更不稳定。
So, along with all the other reasons to keep trim, there is a new one: it may help to keep you free of cancer.
因此，和其他保持苗条的所有理由一道，今天多了一条：保持苗条有助于远离癌症。
