Seconds of 'fat gene' keeps you hungry

Genes have a significant effect on how much and what types of food we eat, new research has revealed.

We know that possessing certain forms of a gene known asFTO(the 'fat mass and obesity-associated gene') predisposes carriers to weight gain. People who have two copies of the high-risk 'A' form of the gene are 1.7 times more likely to become obesethan those who carry two copies of the low-risk 'T' form - why this happens wasn't known.

Now, a new study from a UCL-based team led by Rachel Batterham, has shed light on how this gene promotes weight gain.

FTOgene, they have discovered, interacts directly with a hunger hormone called ghrelin. This is produced by the gut when it becomes empty. Levels of ghrelin in individuals with two copies of the T form of theFTOgene - referred to as TT -plummet after eating, letting the brain and body know that it has been fed. But, individuals with two copies of the A form of the gene - known as AA - experience a fall in ghrelin that is only around half as big. Consequently, AA individuals tend not to feel as satisfied by a meal as TT individuals, which might encourage them to continue eating for longer, or to become tempted to snack soon after.

The UCL team made the discovery by using an MRI scanner to compare the brain activity of AA and TT individuals, both when they had fasted overnight and when they had just eaten. Whilst in the scanner, the subjects were shown pictures of both high and low calorie foods, as well as non-food "control" items.

The results were striking - the responses to food images were dramatically different between the two groups. In the fasted state, both groups responded differently to food images over non-food items. When fed, the TT group showed significant brain activity in response to high-calorie foods, but little response to low-calorie foods; this phenomenon is known as the 'dessert effect'. In contrast, the AA group showed a high response to both high and low calorie foods, particularly in areas of the brain associated with food reward. Broadly, this means that AA individuals might be less picky about what they eat after a meal than TT carriers, and so might be tempted to eat more.

Batterham's group then looked at what effect ghrelin levels themselves had on brain response to the images. In the fed state, as ghrelin levels decreased, members of the TT group had a decreased response to food. But the complete opposite was observed in AA individuals who, as ghrelin levels decreased, showed an increase in brain activity in incentive-related brain areas, particularly in response to high calorie foods.

These findings suggest that there is an intrinsic difference in the way that the brains of AA and TT individuals respond to food. This difference in perception of food and hunger might cause carriers of the A form of theFTOgene to overeat and gain weight in a way that carriers of the T form do not.

Although this is by no means a complete answer, this study brings us one step closer to understanding the causes of obesity and how it might be targeted in the future.