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Sicience and technology
科學和技術
Cancer and obesity
癌癥與肥胖
Malignant flab
惡性松弛
At last, an understanding of how overeating causes cancer
吃得過多如何導致癌癥
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.
原因一直以來都是個迷。
But it is now less mysterious thanks to the work of Kevin Gardner, a researcher at America's National Cancer Institute in Bethesda, Maryland.
但由于馬里蘭州美國國家癌癥協會研究院KG研究員為此做出的努力，現在并沒有之前那么神秘了。
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博士和他的同事們發現合成卡路里的過程會影響BRCA1基因的活性，該基因為一種著名的抗腫瘤蛋白質編碼。
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基因的突變是乳癌和卵巢癌的強烈預報器---如此強烈以至于在美國，常常就有關自然基因序列是否可以申請專利這樣的問題發生訴訟，因此測試這些突變的市場被壟斷了。
Dr Gardner's discovery is that a substance called C-terminal binding protein helps regulate BRCA1.
KG博士發現了一種能夠調節BRCA1基因的蛋白質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.
因為CtBP蛋白質本身由加工富含卡路里的分子的過程控制著，所以身體處理越多的這類分子，患癌癥的風險就越大。
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蛋白質通過結合一種叫做NADH的小分子來感知每個細胞中的總能量。
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+.
這種化學物質是新陳代謝的副產物，并且那些處理并存儲過剩能量的細胞擁有過剩的NADH分子，
As the ratio of NAD+ to NADH falls, CtBP combines with NADH.
和與之有關叫做NAD+的分子比起來。
This changes CtBP's shape and enables it to form complexes with several other proteins.
這改變了CtBP的形狀并使之形成一種帶有其他蛋白質的聯合體。
These complexes control the activity of DNA by shutting off certain genes.
這些聯合體通過切斷某些基因控制DNA活動。
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博士和他的團隊在最新一期的《自然結構和分子生物》上宣稱，其中這么被控制的基因中就有BRCA1。
The protein encoded by BRCA1 is involved in DNA repair.
被BRCA1基因編碼的蛋白質與DNA修復有關。
Cells that lack a working version of it gradually accumulate genetic changes.
缺乏它的一個工作版本的細胞們漸漸引起了基因的改變。
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.
盡管多數改變要么影響不大，要么會導致細胞死亡，但有些可能會刺激腫瘤的形成或惡化。
A low NAD+/NADH ratio, according to Dr Gardner's work, has a similar effect to a BRCA1 mutation.
據KG博士的研究工作，低水平的NAD+/NADH對BRCA1突變會產生類似作用。
It leads to less DNA repair and more mutations.
這導致了DNA修復的減少卻增加了基因的突變的可能性。
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，這和另外一個過多攝入脂肪的影響就結合起來，過多攝入脂肪通過那些儲存脂肪的細胞會刺激雌激素的產生。更多的雌激素意味著荷爾蒙細胞增殖—這是一種非常敏感的組織—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，當這些細胞被通知經歷可能會出錯的復制和分裂過程并需要他們的DNA修復系統時，CtBP就會將此系統破壞。
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.
盡管這是攝入熱量和癌癥之間聯系的首次清晰描述，該聯系是在分子水平下被發現的，但KG博士說，他的研究結果與之前的大量實驗一致。
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，與那些吃熱量受限制食物的老鼠相比，不加限制的老鼠的乳房腫塊更惡性且基因更不穩定。
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，和其他保持苗條的所有理由一道，今天多了一條：保持苗條有助于遠離癌癥。
