2018-03-03 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.

天然糖類中,果糖最甜。從字面可以看出,果糖主要來源于水果。從進(jìn)化學(xué)來看,果糖的作用貌似是更多地吸引脊椎動物吃果實,使其種子得以分布的更遠(yuǎn)、更廣。然而,食品飲料生產(chǎn)商為了讓產(chǎn)品更甜,也經(jīng)常添加果糖,只為吸引一類特別的脊椎動物,所謂智人。這就帶來一個問題,果糖攝入過量,與肝臟疾病和二型糖尿病可能相關(guān)。

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.

這種相關(guān)性一直有爭議。有些認(rèn)為其作用是間接的,因為甜味道會抑制飽腹感(餐后才上甜點(diǎn)是因為甜),進(jìn)食含有較多果糖的食物,可致過度飲食,繼而誘發(fā)疾病。另一些人認(rèn)為其作用是直接的,病因在于果糖的代謝方式。兩種假說都缺少明確證據(jù)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.

可是這周,普林斯頓大學(xué)的Josh和他的同事們發(fā)表在《細(xì)胞新城代謝》的一篇研究對新城代謝的假設(shè)有所支持。明確的說,Dr.的研究表明,攝入足夠量的果糖將會削弱小腸進(jìn)化而來的處理果糖的機(jī)制。這使得它隨著其他消化的分子進(jìn)入血液,從而進(jìn)入到肝臟,在那里它的一些轉(zhuǎn)換成脂肪。這是一個有可能造成長期損害的過程。?

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博士和他的同事通過跟蹤果糖和葡萄糖,通過小鼠的身體來得出這一結(jié)論。他們的做法是制造糖分子,其中包括一種罕見但非放射性的碳同位素,即13C。一些動物被喂食了摻有這種同位素的果糖。其他的則被喂食了摻有葡萄糖的葡萄糖。通過觀察13C在每種情況下的位置研究人員可以跟蹤這兩種糖的命運(yùn)

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.

肝臟是人體的主要代謝處理中心,所以他們希望看到果糖在這里得到處理。但是同位素講述了一個不同的故事。當(dāng)葡萄糖是被摻雜的糖分子時,從小腸通過肝門靜脈將13C迅速地從小腸運(yùn)送到肝臟。這是兩個器官之間的直接連接,它們是用來進(jìn)行消化的食物分子的轉(zhuǎn)移的。然后通過血液循環(huán)將其分發(fā)給身體的其他部分。然而,當(dāng)果糖被摻雜時,少量的攝入,同位素就會聚集在一起

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.

已經(jīng)確立了兩種糖被(人體)處理的不同方式,接著Rabinowitz博士和他的同事增加劑量。他們給老鼠服用的劑量比例類似于人類在喝略多果糖的軟飲料時所攝入的量。正如他們所料,全部的葡萄糖被高效地輸送到了肝臟,接著葡萄糖被釋放入血液中用來供給全身。同樣和預(yù)期相符的是,果糖會被留在小腸中處理,然而果糖并不是一直殘留著。大約30%的未加工的果糖會逃逸,并且被運(yùn)送到肝臟,在那里,其中一部分的果糖會被轉(zhuǎn)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.

短時間內(nèi)這不成問題,毫無爭議的,肝臟是可以儲存大量脂肪。Rabinowitz博士的實驗也只是短期的,但肝臟的脂肪長久慢性積累確經(jīng)常會產(chǎn)生疾病,如果可能的,這些疾病也是也可以避免的

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