• The faulty MC4R pathway could explain why an obese person may have a heightened taste fatty foods and a weight problem. (Getty Images)Source: Getty Images
A genetic defect could explain why one-in-100 obese people may have a soft spot for fatty foods and little interest in sugary treats, according to new research.
By
Yasmin Noone

5 Oct 2016 - 4:25 PM  UPDATED 5 Oct 2016 - 4:43 PM

Obese people with the taste for fatty foods and a dislike of sugary treats may have a rare genetic defect that influences their food choices, according to new findings from the UK.

A University of Cambridge study, published today in the journal Nature Communications, shows that one-in-100 obese people may have a defect in a gene called melanocortin-4 receptor (MC4R).

The researchers think that the faulty MC4R pathway could explain why an obese person may have a heightened taste for fatty foods and a weight problem, even though they have little interest in consuming sugary foods.

“By carefully testing these nutrients separately in this study, and by testing a relatively rare group of people with the defective MC4R gene, we were able to show that specific brain pathways can modulate food preference.” 

“Most of the time we eat foods that are both high in fat and high in sugar,” says research lead, Professor Sadaf Farooqi from the Wellcome Trust–Medical Research Council Institute of Metabolic Science at the University of Cambridge.

“By carefully testing these nutrients separately in this study, and by testing a relatively rare group of people with the defective MC4R gene, we were able to show that specific brain pathways can modulate food preference.”

Senior researcher at Neuroscience Research Australia, Associate Professor John Kwok says although some cases of obesity will be explained by the genetic mutation, the variant is still rare.

“Only about one in 100 people who are obese have a defect in the MC4R gene which makes them more likely to put on weight,” says A/Prof Kwok.

“Although some people have a genetic susceptibility to obesity, environment, diet, lifestyle and epigenetics also plays a huge part in determining your weight.”  

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He also explains that not every single person with the mutation will necessarily be obese either as “obesity is an interaction between lifestyle and genetic predisposition to an underlying condition”.

There are many other genes that increase the risk of gaining weight and the impact of these genes on eating behaviour needs to be studied in the future.

“If you know you have a genetic predisposition to obesity, you may just have to be even more aware of your dietary intake patterns.” 

This study is one of the first to show a direct link between food preference and specific genetic variants in humans.

It may even shine a light onto our evolutionary past, highlighting how humans may have evolved pathways in the brain that modulate our preference for high fat food in order to cope with famine.

“When there is not much food around, we need energy that can be stored and accessed when needed: fat delivers twice as many calories per gram as carbohydrates or protein and can be readily stored in our bodies,” Professor Sadaf Farooqi explains.

“As such, having a pathway that tells you to eat more fat at the expense of sugar, which we can only store to a limited extent in the body, would be a very useful way of defending against starvation.”

“Only about one in 100 people who are obese have a defect in the MC4R gene which makes them more likely to put on weight." 

The researchers tested lean people, obese people, and those living with obesity known to have the defect MC4R by giving them an all-you-can-eat chicken korma buffet.

Although all the dishes the same, the buffet boasted three korma options, which varied according to fat content: 20, 40 or 60 per cent fat.

It found that individuals with defective MC4R ate almost double the amount of high fat korma than lean individuals ate and 65 per cent more than obese individuals.

Study participants were then given Eton mess – a dessert that includes a mixture of strawberries, whipped cream and broken meringue.

Again, there were three options from which participants could freely choose, with sugar content providing low, medium and high calorific content, but with the fat content fixed.

Results showed that lean and obese individuals without the defect said they liked the high sugar Eton mess more than the other two desserts, while participants with defective MC4R didn’t like the high sugar dessert as much as the other less the other participants.

Those with the defect ate significantly less of all three desserts compared to the other two groups.

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