[考研英语]英语翻译及阅读资料-经济学人7.pdf
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1、Metabolic syndrome代谢综合症A game of consequences?因果游戏?One of the scourges of modern life may have been profoundly misunderstood现代生活中的一大祸害或许被深深地冤枉了Mar 11th 2010 I From The Economist print editionBEING fat is bad for you.On that,almost everyone agrees.It is just possible,though,that almosteveryone is wro
2、ng.In fact,getting fat may be a mechanism that protects the body.The healthproblems associated with fatness may not be caused by it but be another consequence,anothersymptom,of overeating.长得胖对你可一点儿都不好,几乎每个人都这么认为。然而,可能每个人都错了。实际上,发胖可能是保护身体的方法。与肥胖有关的健康问题或许并不是肥胖本身引起的,而是暴饮暴食的又一个后果,又一个症状。That is the heret
3、ical proposal of Roger Unger and Philipp Scherer.Dr Unger and Dr Scherer,whowork at the University of Texas,in Dallas,have been reviewing the science of what has come tobe known as metabolic syndrome.This is a cluster of symptoms such as high blood pressure,insulin resistance and fatness that seem t
4、o increase the risk of heart disease and strokes,late-onsetdiabetes and liver disease.Metabolic syndrome is found in a sixth of the American population这正是罗杰昂格尔和菲利普谢勒提出的颠覆传统的观点。一直以来,德克萨斯大学达拉斯分校的昂格尔博士和谢勒博士都在进行被称为代谢综合症的科学研究。代谢综合症是一系列症状,比如高血压、胰岛素抵抗和肥胖,这些症状似乎会增加心脏病和中风、晚发型心脏病和肝病的患病风险。美国六分之一的人都患有代谢综合症。“Syn
5、drome“is the medical term for a collection of symptoms whose common cause is notproperly understood.The symptom of metabolic syndrome that appears first is usually obesity,sothis is generally regarded as the underlying cause.“综合症”是一个医学术语,表示一系列的症状,而导致这些症状的共同原因没有得到正确地理解。代谢综合症最先出现的症状通常为肥胖,因而肥胖一般被视为其根本起
6、因。Dr Unger and Dr Scherer,however,turn this logic on its head.They point out that there is usuallya period of many years between a person becoming overweight and his developing the othersymptoms.If the growth of adipose tissue(the body cells in which fat is stored)were directlyharmful,that would not
7、 be the case.This is one of the lines of evidence that has led them to theconclusion that,in addition to its role in storing energy as a hedge against future famine,gettingfat is a protective mechanism against metabolic syndrome.然而,昂格尔和谢勒博士颠覆了这一逻辑。他们指出,一个人从开始发胖到出现其他症状,中间往往隔着很多年的时间。如若脂肪组织(人体贮藏脂肪的细胞)的
8、增长是直接有害的,那事情就不会是这样了。这是系列证据之一,根据这些证据,他们得出了这个结论:除了能够为预防未来的饥饿而储存脂肪之外,发胖也是抵御代谢综合症的一个保护性机制。Their thesis is that lipids(the group of molecules that includes fats),which are needed in smallamounts to make cell membranes,are toxic in larger quantities.Absorbing them into adiposetissue is one of the bodys wa
9、ys of dealing with that toxicity.But are lipids toxic?In one sense,itis obvious that they are.The build up of fatty plaques in blood vessels,which results inatherosclerosis,is a result of the inability of the cells lining the walls of these vessels to cope withtoo much fat.人体需要很少量的脂质(含脂肪的分子群)构成细胞膜,脂
10、质过多是则有毒的,这是他们的论点。将脂质吸收到脂肪组织是人体处理这种毒性的一种途径。不过,脂质真的有毒吗?从某种意义上来说,显然是的。血管中脂肪斑块的堆积会导致动脉粥样硬化,而它则是由构成血管壁的细胞无法处理过多的脂肪造成的。Fat,and proud of it以胖为荣More subtly,though,the two researchers have dug up evidence that an excess of lipids damagesheart-muscle cells,and even destroys pancreatic cells in rodents.This co
11、uld help explain the factthat the form of diabetes that follows metabolic syndrome can involve damage to pancreatic cells.然而,这两位研究者更加敏锐地发现了脂质过多能破坏啮齿目动物的心肌细胞,甚至摧毁其胰腺细胞的证据。这有助于解释为什么在代谢综合症之后出现的糖尿病症会造成对胰腺细胞的损伤。It is generally thought that the growth of adipose tissue causes cells in the liver,muscle and
12、 fattissue to become resistant to insulin(a hormone produced in the pancreas)and thus unable toabsorb glucose from the blood.How this happens has been the subject of a lot of hand waving,though the tendency of adipose tissue to produce chemicals that encourage inflammation is oftenmentioned.专业人士一般都认
13、为脂肪组织的增长会造成肝、肌肉和脂肪组织对胰岛素(胰腺分泌的一种激素)产生抵抗,从而无法吸收血液里的葡萄糖。这一现象的发生一直是一个扑朔迷离的话题,但是脂肪组织倾向于产生恶化炎症的化学物质这一点却经常被提及。Dr Unger and Dr Scherer attack this whole notion.In a paper in Trends in Endocrinology andMetabolism they argue that insulin resistance is another side-effect of metabolic syndrome whosecause is l
14、ipid molecules poisoning tissues in which they are not supposed to be present in largequantities.The problem of lipid damage,they believe,is linked to hormones produced not by thepancreas,but by adipose tissue itself.These hormones are called leptin and adiponectin.昂格尔和谢勒博士反驳了这一整个观念。在刊登在 内分泌学和新陈代谢趋势
15、的 片文章中,他们驳斥道,胰岛素抵抗是代谢综合症的另一个副作用,代谢综合症又是由脂质分子破坏它们所在的组织造成的,而脂质分子不应在这些组织中大量存在。他们认为,脂质的破坏性与激素有关,这些激素不是由胰腺分泌的,而是由脂肪组织本身分泌的。它们被称为瘦素和脂联素。Leptin has several roles,but one is to encourage cells to oxidise lipids and thus destroy them.Forexample,in the cases of the heart-muscle cells and pancreatic cells ment
16、ioned above,dosing themwith leptin keeps them healthy.Adiponectin,meanwhile,encourages the bodys adipose tissue toabsorb lipids.瘦素扮演着几个角色,而其中一个就是刺激细胞氧化脂质从而摧毁它们。例如,以上血提到的心肌细胞和胰腺细胞来说,给这些细胞注入瘦素可以使它们保持健康。而脂联素则刺激人体的脂肪组织吸收脂质。As adipose tissue grows,however,its production of adiponectin falls.The ability o
17、f the tissue toabsorb lipids and keep the rest of the body safe thus drops.Leptin production,meanwhile,growsalong with the mass of the adipose tissue.In what is,admittedly,the least-tested part of their thesis,Dr Unger and Dr Scherer argue that other cells react to this increase in leptin concentrat
18、ion bybecoming resistant to the hormones effects.That,in turn,stops them oxidising lipids and opensthose cells to lipids9 toxic effects.然而,随着脂肪组织的增加,它分泌脂联素的数量会减少。因而脂肪组织吸收脂质、保持身体其他部位的安全的能力也跟着下降。同时,瘦素的分泌量却随着脂肪组织的增加而增加。昂格尔和谢勒博士的理论中有一部分证据最为不充分,在这一部分中,他们称其他细胞会对瘦素的累积产生反应,开始对激素的作用产生抵抗,从而不再对脂质进行氧化,是它们受到脂质毒性
19、的攻击。Dr Unger and Dr Scherer suggest that this failure of the leptin mechanism,particularly its role inoxidising lipids,is crucial to the development of metabolic syndrome,and that it is a pathology ofadipose tissue that has become overloaded.昂格尔和谢勒博士认为瘦素的刺激机制,尤其是在氧化脂质中的角色,的失效,对代谢综合症的发展至关重要,并且这是脂肪组织负
20、荷过重的一个症状。In light of all this,they suggest that insulin resistance,like obesity,should be viewed not as apathology but as an adaptive response by the body to an excess of circulating lipids.To savethemselves when they are threatened with being overwhelmed by lipids,cells becomeinsulin-resistant,whic
21、h stops them taking up extra glucose which would then be converted intolipids.根据这一切,他们认为正如肥胖一样,胰岛素抵抗不应被视为一个症状,而应被视为人体对流通的脂质过量的适应性反应。当细胞受到过量的脂质的威胁时,为了保护自己,它们对胰岛素变得抗拒,从而可以阻止它们吸收多余的葡萄糖,从而阻止这些葡萄糖被转化为脂质。In support of this hypothesis,the researchers point to studies on mice whose leptin receptors havebeen
22、 broken by genetic mutations.In a healthy mouse(one with working leptin receptors)even adiet that is 60%fat does not cause a build-up of lipids anywhere except in the adipose tissue.Inone with broken receptors,a mere 6%is enough to overload other tissues to the point where lipidswould be toxic.Such
23、experiments cannot,of course,be done on people,but something similaroccurs naturally.A few unfortunates are bom without adipose tissue.These people rapidly developthe symptoms of metabolic syndrome.为了支持这一假说,两位研究者提及对老鼠的研究,这些老鼠的瘦素受体因基因突变而受到破坏,在一个健康的老鼠(有正常的瘦素受体)体中,即使吃了含60%的脂肪的食物,除了脂肪组织以外的任何地方都不会产生脂质的积累
24、。但是在受体受损的老鼠体中,哪怕饮食中的脂肪含量只有6%,也足够使其他组织中的脂质多到产生毒性。当然,这样的实验不能在人身上进行,不过,有的人天生就出现了类似的情况。一些不幸的人生来就没有脂肪组织,他们身上很快就出现了代谢综合症的症状。Sadly for self-indulgent humans,none of this affects the basic message about staying healthy,which remains to eat less and exercise more.It does,though,raise important questions abou
25、t howmetabolic syndrome is treated.The focus that many doctors have on controlling diabetes may bemistaken,possibly counterproductive,if insulin resistance is actually a protective mechanism.Even if it is not,the destruction of pancreatic cells that comes with diabetes may be unrelated tothe develop
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