TIME Health For more, visit TIME Health 
 
 Scientists have figured out the reason fiber is such a wonder food: It contains an anti-appetite molecule called acetate. 
 
 Acetate, the researchers discovered, is naturally released when fiber is digested in the gut, and when it’s released, it is taken to the brain where it signals us to stop eating. 
 
 Fiber has long been known to satiate appetite and keep us full for longer, but previous research supposed the reason was that it takes longer to digest, keeping us satisfied for longer after we’ve stopped eating. But this new research published in the journal Nature Communications shows that the acetate released when we digest roughage lowers our appetites when it gets directly into our bloodstream, colon or brain. 
 
 The researchers looked at a dietary fiber called inulin, which comes from chicory and sugar beets, and is often present in cereal bars. They fed mice a diet high in fat with additional inulin. These mice ate less and gained less weight than mice who did not consume inulin, and when the scientists took a deeper look, they discovered that the inulin-eating mice had higher levels of acetate in their gut. So, they used PET scans to track the inulin through the mice. 
 
 They discovered that the acetate traveled from the colon to the liver and heart, and finally made it to the the area of the brain that deals with hunger, the hypothalamus region. Using more imaging, they determined that the acetate accumulates and spurs chemical reactions in the brain that send signals that suppress hunger. 
 
 Eating more fiber, found in foods like nuts, oatmeal, beans, lentils, apples and blueberries, is one of the better ways to feel full and satisfied, and can help with weight management. Science says so. ||||| A pill that switches off hunger is on the horizon after scientists discovered an ‘anti-appetite’ molecule which tells the body to stop eating. 
 
 Researchers at Imperial College discovered that people feel full when eating fruit and vegetables because fibre releases acetate into the gut. 
 
 They believe that a pill derived from acetate could be created to help people cut down on food without experiencing any cravings. 
 
 One in four adults in England is obese and that figure is set to climb to 60 per cent of men and 50 per cent of women by 2050. 
 
 Obesity and diabetes already costs the UK over £5billion every year which is likely to rise to £50 billion in the next 36 years. 
 
 Large amounts of acetate are released when plants and vegetables are digested by bacteria in the colon. The scientists tracked the molecule and found that it eventually ended up in the hypothalamus region of the brain, which controls hunger. 
 
 The new study suggests obesity has become an epidemic because we have replaced the healthy diet of the past with processed food, which does not react with gut bacteria to produce acetate. So the brain does not receive a signal telling it to stop eating. 
 
 The average diet in Europe today contains about 15 g of fibre per day. In Stone Age times it was around 100g per day. 
 
 "Unfortunately our digestive system has not yet evolved to deal with this modern diet and this mismatch contributes to the current obesity epidemic,” said Professor Gary Frost, of Imperial College. 
 
 Although scientists say their research should encourage more people to eat more fruit and vegetables, they also believe it could pave the way for new drugs to help dieters. 
 
 Prof Frost added: "Our research has shown the release of acetate is central to how fibre suppresses our appetite and this could help scientists tackle overeating. 
 
 "The major challenge is to develop an approach that will deliver the amount of acetate needed to suppress appetite but in a form that is acceptable and safe for humans. 
 
 "Developing these approaches will be difficult but it is a good challenge to have and we are looking forward to researching possible ways of using acetate to address health issues around weight gain.” 
 
 The study analysed the effects of a form of dietary fibre called inulin which comes from chicory and sugar beets and is also added to cereal bars. 
 
 Experiments on mice found those fed on a high fat diet with added inulin ate less and gained less weight than animals given a lot of fat diet with no inulin. 
 
 They also noticed that the acetate acculmulates in the hypothalamus of the brain where it triggers a series of chemical events which fire neurons and suppress hunger. 
 
 The research also showed when acetate was injected into the bloodstream, the colon or the brain it reduced the amount of food eaten by the mice. 
 
 Prof Jimmy Bell, of the Medical Research Council, Cambridge, who collaborated in the research, said: "It is exciting we have started to really understand what lies behind fibre's natural ability to suppress our appetite and identified acetate as essential to the process. 
 
 "In the context of the growing rates of obesity in western countries, the findings of the research could inform potential methods to prevent weight gain." 
 
 Acetate is only active for a short amount of time in the body so an ‘acetate pill’ would need to be able to mimic the chemical’s slow release into the gut. 
 
 Prof David Lomas, chair of the MRC's population and systems medicine board, said it is becoming increasingly clear the interaction between the gut and the brain plays a key role in controlling how much food we eat. 
 
 He added: "Being able to influence this relationship, for example using acetate to suppress appetite, may in future lead to new, non surgical treatments for obesity." ||||| Peter Cade/Getty 
 
 A study of mouse metabolism suggests that a product of fibre fermentation may be directly affecting the hypothalamus, a region of the brain involved in regulating appetite. 
 
 People have long been told that a diet high in fibre can help to fight obesity, but how it does so has been unclear. “There has been lots of epidemiological information showing a relationship between fibre and obesity, but no one has been able to connect the epidemiological results with actual mechanisms,” says Jimmy Bell, a biochemist at Imperial College London who worked on the research, published today in Nature Communications1. 
 
 Until now, a high-fibre diet was thought to help keep weight down by stimulating the release of appetite-suppressing hormones in the gut2, says Bell, but humans do not seem to show the same increase in these hormones that mice do. 
 
 So Bell and his colleagues decided to look elsewhere. An obvious candidate, they thought, might be one of the products of fibre fermentation in the gut. In particular they focused on the short-chain fatty acid acetate, because it is the most abundant and is known to circulate throughout the bloodstream. 
 
 They fed mice fibre labelled with carbon-13, which has an additional neutron from the more common carbon-12 that gives its nuclei a magnetic spin and therefore makes it easy to track as it progresses through the body's chemical reactions. The fibre was fermented as usual into acetate, which turned up not only in the gut, but also in the hypothalamus, a part of the brain known to be involved in regulating appetite. There, the researchers found, it was metabolized through the glutamine-glutamate cycle, which is involved in controlling the release of neurotransmitters associated with appetite control. The same model has been proposed for acetate metabolism after drinking alcohol. 
 
 The mice fed with large doses of fermentable fibre ate less food, and ended up weighing less than control mice that were fed unfermentable fibre. 
 
 'Simplistic' approach 
 
 William Colmers, an electrophysiologist who studies the effect of neurotransmitters in the hypothalamus at the University of Alberta in Edmonton, Canada, says he thinks that the experimental work is solid, but worries that the results have been over-interpreted. “Much of it is extremely speculative,” he says. For one thing, the dietary fibre levels were around 11%. At that level, “the room would be full of mouse farts”, he says, so the animals may simply have been eating less because they were uncomfortable. 
 
 Colmers adds that the hypothesis of how acetate in the hypothalamus was affecting the release of neurotransmitters to decrease appetite is “a simplistic view of how the nervous system works”. The release of neurotransmitters is “excruciatingly well regulated”, he says, and not as sensitive to manipulation by changes in biochemistry as the authors suggest. 
 
 Although the work was done in mice, Bell says that he sees “no reason” why the same mechanism shouldn’t be at work in humans. “Acetate is known to be metabolized in the human brain, and we have the right microbiota in our gut for the fermentation of fibre,” he says. 
 
 Bell and his colleagues are preparing to test their ideas in people. The question, however, is how much fibre do you have to eat? Most people's diet contains between 10 and 20 grams of fibre a day, and it can be difficult to increase this amount substantially. So Bell and his colleagues are working with companies that are looking into enriching fibre with acetate to boost the digestive system, and into ways of encasing acetate in nanoparticles so that it releases slowly throughout the day to help control appetite. “It’s sort of a way of having your cake, and not eating it,” says Bell.
– Experts have long suggested that fiber keeps us feeling full because it takes a long time to digest, but new research challenges that notion—and may point the way to a new anti-hunger pill. The key is a short-chain fatty acid called acetate, which emerges as fiber is digested. Acetate then makes its way to the brain's hypothalamus, where it builds up and triggers chemical reactions that tell us we're full, Time reports. Researchers reached this conclusion by scanning the progress of a dietary fiber called inulin through the bodies of mice. Those mice who ate fatty diets rich in inulin gained less weight than mice who didn't eat inulin. But one electrophysiologist not related to the study points out that the mice were fed dietary fiber levels of about 11%. He tells Nature that at such a level, "the room would be full of mouse farts"—and perhaps the mice were eating less because they felt gassy. The researchers plan to next test the idea in humans. So could we eventually see an acetate-based diet pill? It's possible, the Telegraph suggests: "The major challenge is to develop an approach that will deliver the amount of acetate needed to suppress appetite but in a form that is acceptable and safe for humans," a researcher says.