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.

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.

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.

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.

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.

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.

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.