By Bianca Nogrady
Can’t resist a chicken korma but pass up on a sweet dessert?
The study, published today in Nature Communications, looked at the effect on human dietary preferences of a mutation in the gene for the melanocortin-4-receptor (MC4R).
The MC4R is found on nerves in the brain, and influences what we like to eat and how much we eat.
“Our work shows that even if you tightly control the appearance and taste of food, our brains can detect the nutrient content,” said lead researcher Professor Sadaf Farooqi, of University of Cambridge.
Defects in the MC4R gene are found in around 1–5 per cent of obese individuals, resulting in severe obesity with an early age of onset.
Earlier studies in mice have shown that disrupting the action of this receptor makes the mice eat more food but specifically high-fat food rather than sweet food.
In this study, the researchers presented a group of 14 people — some lean, some obese, and some with a genetic variant of the MC4R gene — with an all-you-can-eat buffet featuring low, medium and high-fat versions of the same chicken korma dish.
After first giving everyone a taste-test of each dish and getting them to score their liking of each, the team let the group eat as much as they wanted from whatever dish.
While the liking scores for the low, medium and high-fat meals were similar across all the participants, those with the defective MC4R ate almost double the amount of the high-fat meal compared to the lean participants, and 65 per cent more than the obese individuals without the defective receptor.
In a second test, researchers did the same thing but this time, instead of the low, medium or high-fat chicken korma, they used low, medium or high-sugar versions of Eton mess; a dessert of meringue, whipped cream and strawberries.
This time, the lean and obese volunteers liked the high-sugar version of the dessert much more than the individuals with the defective MC4R, who also ate far less of the higher-sugar Eton mess.
Drive to eat not purely a matter of self-control.
Commenting on the findings, Associate Professor Amanda Salis said the study was important because it showed that the drive to eat was not purely a matter of self-control and discipline.
“This study is really nice in that it’s shown in carefully controlled scientific way that people who do have certain genetic variations are driven to eat fattier, more substantial energy-dense foods which tend to promote weight gain,” said Professor Salis, of the University of Sydney’s Boden Institute of Obesity, Nutrition, Exercise & Eating Disorders at the Charles Perkins Centre.
Professor Salis said the MC4R was part of a system that evolved to help us survive during a famine by driving us to seek out high-fat foods, instead of high-carbohydrate or sugar foods which offer a lower energy return.
“In these people who have a mutation in the melanocortin-4-receptor, that pathway is permanently blocked so it’s like they’re permanently in the state of this famine reaction,” Professor Salis said.
“They constantly have this drive to eat and this study shows that it is a stronger drive to eat not everything, but specifically food that contains fat.”
Professor Salis said several groups of researchers around the world were looking for ways to target the MC4R as a way to not only help people with a defective version, but also help with weight loss generally.
This post originally appeared on ABC News.
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