2018.3.3 How too much fructose may cause liver damage

Fructose is the sweetest of the natural sugars. As its name suggests, it is found mainly in fruits. Its job seems to be to appeal to the sweet tooths of the vertebrates these fruit have evolved to be eaten by, the better to scatter their seeds far and wide. Fructose is also, however, often added by manufacturers of food and drink, to sweeten their products and make them appeal to one species of vertebrate in particular, namely Homo sapiens. And that may be a problem, because too much fructose in the diet seems to be associated with liver disease and type 2 diabetes.
天然糖类中，果糖最甜。从字面可以看出，果糖主要来源于水果。从进化学来看，果糖的作用貌似是更多地吸引脊椎动物吃果实，使其种子得以分布的更远、更广。然而，食品饮料生产商为了让产品更甜，也经常添加果糖，只为吸引一类特别的脊椎动物，所谓智人。这就带来一个问题，果糖摄入过量，与肝脏疾病和二型糖尿病可能相关。

The nature of this association has been debated for years. Some argue that the effect is indirect. They suggest that, because sweet tastes suppress the feeling of being full (the reason why desserts, which come at the end of a meal, are sweet), consuming foods rich in fructose encourages overeating and the diseases consequent upon that. Others think the effect is more direct. They suspect that the cause is the way fructose is metabolised. Evidence clearly supporting either hypothesis has, though, been hard to come by.
这种相关性一直有争议。有些认为其作用是间接的，因为甜味道会抑制饱腹感(餐后才上甜点是因为甜)，进食含有较多果糖的食物，可致过度饮食，继而诱发疾病。另一些人认为其作用是直接的，病因在于果糖的代谢方式。两种假说都缺少明确证据支持。
This week, however, the metabolic hypothesis has received a boost from a study published in Cell Metabolism by Josh Rabinowitz of Princeton University and his colleagues. Specifically, Dr Rabinowitz’s work suggests that fructose, when consumed in large enough quantities, overwhelms the mechanism in the small intestine that has evolved to handle it. This enables it to get into the bloodstream along with other digested molecules and travel to the liver, where some of it is converted into fat. And that is a process which has the potential to cause long-term damage.
可是这周，普林斯顿大学的Josh和他的同事们发表在《细胞新城代谢》的一篇研究对新城代谢的假设有所支持。明确的说，Dr.的研究表明，摄入足够量的果糖将会削弱小肠进化而来的处理果糖的机制。这使得它随着其他消化的分子进入血液，从而进入到肝脏，在那里它的一些转换成脂肪。这是一个有可能造成长期损害的过程。
Dr Rabinowitz and his associates came to this conclusion by tracking fructose, and also glucose, the most common natural sugar, through the bodies of mice. They did this by making sugar molecules that included a rare but non-radioactive isotope of carbon, 13C. Some animals were fed fructose doped with this isotope. Others were fed glucose doped with it. By looking at where the 13C went in each case the researchers could follow the fates of the two sorts of sugar.
Rabinowitz博士和他的同事通过跟踪果糖和葡萄糖，通过小鼠的身体来得出这一结论。他们的做法是制造糖分子，其中包括一种罕见但非放射性的碳同位素，即13C。一些动物被喂食了掺有这种同位素的果糖。其他的则被喂食了掺有葡萄糖的葡萄糖。通过观察13C在每种情况下的位置研究人员可以跟踪这两种糖的命运

The liver is the prime metabolic processing centre in the body, so they expected to see fructose dealt with there. But the isotopes told a different story. When glucose was the doped sugar molecule, 13C was carried rapidly to the liver from the small intestine through the hepatic portal vein. This is a direct connection between the two organs that exists to make such transfers of digested food molecules. It was then distributed to the rest of the body through the general blood circulation. When fructose was doped, though, and administered in small quantities, the isotope gathered in the small intestine instead of being transported to the liver. It seems that the intestine itself has the job of dealing with fructose, thus making sure that this substance never even reaches the liver.

肝脏是人体的主要代谢处理中心，所以他们希望看到果糖在这里得到处理。但是同位素讲述了一个不同的故事。当葡萄糖是被掺杂的糖分子时，从小肠通过肝门静脉将13C迅速地从小肠运送到肝脏。这是两个器官之间的直接连接，它们是用来进行消化的食物分子的转移的。然后通过血液循环将其分发给身体的其他部分。然而，当果糖被掺杂时，少量的摄入，同位素就会聚集在一起

Having established that the two sorts of sugar are handled differently, Dr Rabinowitz and his colleagues then upped the doses. Their intention was to mimic in their mice the proportionate amount of each sugar that a human being would ingest when consuming a small fructose-enhanced soft drink. As they expected, all of the glucose in the dose was transported efficiently to the liver, whence it was released into the wider bloodstream for use in the rest of the body. Also as expected, the fructose remained in the small intestine for processing. But not forever. About 30% of it escaped, and was carried unprocessed to the liver. Here, a part of it was converted into fat.
已经确立了两种糖被(人体)处理的不同方式，接着Rabinowitz博士和他的同事增加剂量。他们给老鼠服用的剂量比例类似于人类在喝略多果糖的软饮料时所摄入的量。正如他们所料，全部的葡萄糖被高效地输送到了肝脏，接着葡萄糖被释放入血液中用来供给全身。同样和预期相符的是，果糖会被留在小肠中处理，然而果糖并不是一直残留着。大约30%的未加工的果糖会逃逸，并且被运送到肝脏，在那里，其中一部分的果糖会被转化成脂肪。

That is not a problem in the short term. Livers can store a certain amount of fat without fuss. And Dr Rabinowitz’s experiments are only short-term trials. But in the longer term chronic fat production in the liver often leads to disease—and is something to be avoided, if possible.
短时间内这不成问题，毫无争议的，肝脏是可以储存大量脂肪。Rabinowitz博士的实验也只是短期的，但肝脏的脂肪长久慢性积累确经常会产生疾病，如果可能的，这些疾病也是也可以避免的