Obesity may be genetically linked to how our bodies digest carbohydrates, according to a new study from Imperial College London.

The body uses carbohydrates from the food we eat to produce glucose, which is used to fuel bodily functions. The human body can either use this glucose right away or store it in the liver and muscles for when it’s needed.

In their study, published Nature Genetics, researchers examined the connection between body weight and a gene called AMY1,which produces an enzyme found in our saliva called salivary amylase. The enzyme goes to work as soon as we take our first bite; it’s one of the first steps the body takes to digest starchy food.

Usually our DNA contains two copies of this gene, but researchers have found that various regions throughout our DNA can carry any number of the AMY1 gene and that the quantity of this gene can also vary between different people. The researchers believe that the higher numbers of AMY1 found in humans today is an evolutionary response to the change in diets toward increased starch.

Working with colleagues at institutions in other parts of the world, the British researchers looked into the number of AMY1 copies present in the DNA of people from the UK, France, Sweden and Singapore.

The UK scientists began their research project by first analyzing genetic data from 481 members of a Swedish family. The family participants were selected by sibling pairs, where one was obese and the other was not.

The researchers used this data to develop a short list of genes whose differences in numbers within an individual’s DNA influenced that person’s body mass index (BMI). In analyzing this list, the scientists found the gene coding for the AMY1 gene was the one with the greatest influence on body weight.

With this finding in hand, they went on study about 5,000 more test subjects from France and the UK and looked into the association between the number of times the AMY1 gene was repeated on chromosome 1 in each of these people and their risk of obesity.

After checking for the amount of AMY1 copies contained in their test subject’s DNA, they noticed that those with a low number of the salivary enzyme producing gene had a greater chance of becoming obese.

The researchers then expanded their study to include approximately 700 people from Singapore, both obese and normal weight, and came up with the same results found with the European subjects.

The UK scientists found that people with fewer than four copies of the AMY1 had a nearly eight times higher chance of being obese that those who had nine or more copies within their DNA.

With every extra copy of the AMY1 gene a person had, the researchers estimated that there was approximately a 20 per cent decrease in the chances of that person becoming obese.

“I think this is an important discovery because it suggests that how we digest starch and how the end products from the digestion of complex carbohydrates behave in the gut could be important factors in the risk of obesity,” said Philippe Froguel of Imperial College London, one of the study’s lead authors. “Future research is needed to understand whether or not altering the digestion of starchy food might improve someone’s ability to lose weight, or prevent a person from becoming obese.”

The team is also interested in whether there’s a link between this genetic variation and people’s risk of other metabolic disorders such as diabetes.

Another study author, Mario Falchi, also from Imperial College London, said that while their study examined how our bodies physically digest carbohydrates, earlier genetic studies related to obesity focused on identifying differences in genes that act in the brain which control our appetites.

He said that the previous studies, combined with their new research, will allow scientists to find better ways of attacking obesity.

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