Metabolic syndrome
代谢综合症
A game of consequences?
意义深远的博弈？
One of the scourges of modern life may have been profoundly misunderstood
现代生活方式带来的一种灾难也许是源自彻底的误解
Mar 11th 2010 | From The Economist print edition
BEING fat is bad for you. On that, almost everyone agrees. It is just possible, though, that almost everyone is wrong. In fact, getting fat may be a mechanism that protects the body. The health problems associated with fatness may not be caused by it but be another consequence, another symptom, of overeating.
发胖对你不利。关于这一点，几乎人人赞成。然而，他们几乎都错了却是非常可能的。事实上，发胖可能是一种保护身体的途径。与肥胖的健康相关的问题可能不是由发胖引起的，而是另一种症状-暴饮暴食-引起的后果。
That is the heretical proposal of Roger Unger and Philipp Scherer. Dr Unger and Dr Scherer, who work at the University of Texas, in Dallas, have been reviewing the science of what has come to be known as metabolic syndrome. This is a cluster of symptoms such as high blood pressure, insulin resistance and fatness that seem to increase the risk of heart disease and strokes, late-onset diabetes and liver disease. Metabolic syndrome is found in a sixth of the American population.
这就是Roger Unger罗杰•昂格尔和Philipp Scherer（菲利普•谢勒）标新立异的新提法。昂格尔博士和谢勒博士在达拉斯的德州大学工作。他们评估了被归结为代谢综合症的这个学科。这是一组症状，诸如高血压，胰岛素耐受性以及肥胖。肥胖似乎容易导致心脏病，中风，迟发性糖尿病以及肝脏疾病等等。在美国，六分之一的成年人患有代谢综合症。
“Syndrome” is the medical term for a collection of symptoms whose common cause is not properly understood. The symptom of metabolic syndrome that appears first is usually obesity, so this is generally regarded as the underlying cause.
“综合症”是一个适用于还不为人准确认识其共同的引发原因的一系列症状的医学名词。代谢综合症的症状首次出现时，通常表现为肥胖。因此，肥胖被普遍认为是代谢综合症最主要的病因。
Dr Unger and Dr Scherer, however, turn this logic on its head. They point out that there is usually a period of many years between a person becoming overweight and his developing the other symptoms. If the growth of adipose tissue (the body cells in which fat is stored) were directly harmful, that would not be the case. This is one of the lines of evidence that has led them to the conclusion that, in addition to its role in storing energy as a hedge against future famine, getting fat is a protective mechanism against metabolic syndrome.
然而，昂格尔博士和谢勒博士完全推翻了这种逻辑。他们指出，通常在一个人变得过重以及产生其他症状之前，有长达数年的一段时期。如果脂肪组织（储存脂肪的体细胞）的生长对人体直接有害这个说法和事实不相符合。这也是导致他们得出“发胖除了在为未来的饥饿储备能源中的作用外，还是一种对抗代谢综合症的保护性机制”这一结论的系列证据中的一条。
Their thesis is that lipids (the group of molecules that includes fats), which are needed in small amounts to make cell membranes, are toxic in larger quantities. Absorbing them into adipose tissue is one of the body’s ways of dealing with that toxicity. But are lipids toxic? In one sense, it is obvious that they are. The build up of fatty plaques in blood vessels, which results in atherosclerosis, is a result of the inability of the cells lining the walls of these vessels to cope with too much fat.
他们的论点是少量的脂类（包含脂肪的分子族）是构成细胞膜所必需的。大量的脂类则是（对身体）有毒的。将脂类吸收在脂肪组织是身体处理这些有毒物质的方法之一。但是脂类真的有毒吗？从某种意义上，显然如此。血管中脂肪块的形成导致动脉硬化就是血管壁上排列的细胞无力处理这些多余的脂肪所引起的。
Fat, and proud of it
脂肪，以及为之骄傲
More subtly, though, the two researchers have dug up evidence that an excess of lipids damages heart-muscle cells, and even destroys pancreatic cells in rodents. This could help explain the fact that the form of diabetes that follows metabolic syndrome can involve damage to pancreatic cells.
这两位研究者非常巧妙地找出了过多的脂类破坏啮齿类动物心脏肌肉细胞，甚至破坏胰脏细胞的证据。这也有助于解释这个事实：随着代谢综合症的产生而发生的糖尿病和胰脏细胞的损坏有关。
It is generally thought that the growth of adipose tissue causes cells in the liver, muscle and fat tissue to become resistant to insulin (a hormone produced in the pancreas) and thus unable to absorb 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 often mentioned.
一般来说，人们通常认为脂肪组织的生长导致肝细胞，肌肉细胞以及脂肪细胞对胰岛素（胰腺产生的激素）产生抵抗性，这些细胞因此无法从血液中吸收葡萄糖。这个过程是如何形成的，仍然是很多人正在研究的课题。但是，脂肪组织趋向于产生一种刺激炎症的化学物质的这种提法经常被提起。
Dr Unger and Dr Scherer attack this whole notion. In a paper in Trends in Endocrinology and Metabolism they argue that insulin resistance is another side-effect of metabolic syndrome whose cause is lipid molecules poisoning tissues in which they are not supposed to be present in large quantities. The problem of lipid damage, they believe, is linked to hormones produced not by the pancreas, but by adipose tissue itself. These hormones are called leptin and adiponectin.
昂格尔博士和谢勒博士抨击了这种概念体系。在《内分泌学和代谢学趋势》上发表的论文里，他们提出，insulin resistance（抗胰岛素性）是代谢综合症的另一种副作用，起因在于原本就不应该在组织中出现的大量的脂类分子引起的组织中毒。他们相信，脂类的破坏性和由脂肪组织产生的激素（而不是由胰腺产生的激素）有关。这种由脂肪组织产生的激素被称做leptin（瘦蛋白）和adiponectin（脂肪连接蛋白）。
Leptin has several roles, but one is to encourage cells to oxidise lipids and thus destroy them. For example, in the cases of the heart-muscle cells and pancreatic cells mentioned above, dosing them with leptin keeps them healthy. Adiponectin, meanwhile, encourages the body’s adipose tissue to absorb lipids.
leptin瘦蛋白有几种功效。一种是激励细胞氧化脂类并分解脂类。例如，就上文中提到的心脏细胞以及胰腺细胞而言，给它们分配leptin（瘦蛋白）可以使这些细胞保持健康状态。同时，adiponectin（脂肪连接蛋白）激励身体里的脂肪组织吸收脂类。
As adipose tissue grows, however, its production of adiponectin falls. The ability of the tissue to absorb lipids and keep the rest of the body safe thus drops. Leptin production, meanwhile, grows along 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 concentration by becoming resistant to the hormone’s effects. That, in turn, stops them oxidising lipids and opens those cells to lipids’ toxic effects.
然而，随着脂肪组织的生长，它制造adiponectin（脂肪连接蛋白）的能力下降。脂肪组织吸收脂类的能力以及保持身体其余部分安全的能力也随着下降。同时，leptin（瘦蛋白）的分泌量随着大量的脂肪组织的增加而增加。在他们至少是部分被无可否认地证实的论文中，昂格尔博士和谢勒博士提出，其他细胞对leptin（瘦蛋白）的浓度升高的反应表现在对激素作用的抵抗性的产生。因此，结果使细胞停止氧化脂类，并对脂类的有毒影响无法抵抗。
Dr Unger and Dr Scherer suggest that this failure of the leptin mechanism, particularly its role in oxidising lipids, is crucial to the development of metabolic syndrome, and that it is a pathology of adipose tissue that has become overloaded.
昂格尔博士和谢勒博士指出，leptin（瘦蛋白）机制的失效，尤其是在氧化脂类方面的失效对代谢综合症的发展有着关键性的影响，而且这也是过度负载的脂肪组织的一种病状。
In light of all this, they suggest that insulin resistance, like obesity, should be viewed not as a pathology but as an adaptive response by the body to an excess of circulating lipids. To save themselves when they are threatened with being overwhelmed by lipids, cells become insulin-resistant, which stops them taking up extra glucose which would then be converted into lipids.
基于所有这些原因，他们提出insulin resistance（抗胰岛素性），就象肥胖一样，不应该被视为病症，而应该是身体对过量的在体内循环的脂类的适应性反应。当细胞受大量的压倒性的脂类的威胁时，为保证细胞的安全，细胞对胰岛素产生抵抗性，这使细胞停止吸收可以转化为脂类的过量的葡萄糖。
In support of this hypothesis, the researchers point to studies on mice whose leptin receptors have been broken by genetic mutations. In a healthy mouse (one with working leptin receptors) even a diet that is 60% fat does not cause a build-up of lipids anywhere except in the adipose tissue. In one with broken receptors, a mere 6% is enough to overload other tissues to the point where lipids would be toxic. Such experiments cannot, of course, be done on people, but something similar occurs naturally. A few unfortunates are born without adipose tissue. These people rapidly develop the symptoms of metabolic syndrome.
为了支持他们的假设，研究人员用因基因突变导致leptin（瘦蛋白）受体被破坏的鼠类实验来证明。健康的老鼠（体内的leptin（瘦蛋白）受体有效运作）即使在用含60%脂肪的食物喂养后，除了在脂肪组织之外，并没有引起脂类的积累。体内的leptin（瘦蛋白）受体被破坏的老鼠，仅仅是含6%脂肪的食物喂养就足以使脂类的含量在它体内的其他组织中达到对组织有害的水平。当然，这样的实验不可能把人当做实验对象。但是，有类似的自然发生的案例。有少数不幸的病人，他们出生时体内就没有脂肪组织。这些病人很快就产生代谢综合症的症状。
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 about how metabolic syndrome is treated. The focus that many doctors have on controlling diabetes may be mistaken, 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 to the development of insulin resistance. And liposuction (not, admittedly, something that most doctors would recommend) would be expected to make things worse, since it would get rid of the source of the hormones that regulate lipids.
令人悲哀的是，在过分放纵自我的人类中，几乎无人喜欢这个基本的关乎保持健康的信息，这个信息就包含在少吃多动中。虽然这个信息提出了关于如何治疗代谢综合症的若干重要问题。假如抗胰岛素性确实是一种保护机制，那么很多医生在控制糖尿病时关注的重点或许是错误的，也很可能是会起反作用的。即使这点和事实不符，和糖尿病一起发生的胰腺细胞的破坏也许和抗胰岛素性的产生毫无关联。而抽脂手术（虽然不被公认，但却是大部分医生会推荐的手段）可能会使情况变的糟糕，因为这可能导致调节脂类的激素源被抽走。
Dr Unger and Dr Scherer, then, have attempted to apply some new thinking to a disease that affects more people as the world gets richer. Even if they are wrong, a little lateral thinking may help shake up the field. If they are right, a lot of people may thank them in the future.
因此，昂格尔博士和谢勒博士试图应用一种新的思路来解决这种因世界变的富裕而使更多人受到影响的疾病（也就是代谢综合症）。即便他们是错的，他们的这些横向思考或许能有助于激励这个领域的进步。 如果他们是对的，那么在未来或许会有许许多多的人感谢他们。
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