A new study has reportedly detailed how a common gene variant linked to obesity affects the production and reception of ghrelin, the hormone responsible for stimulating hunger. Efthimia Karra, et al., “A link between FTO, ghrelin, and impaired brain food-cue responsivity,” Journal of Clinical Investigation, July 2013. According to a July 15, 2013, press release, in the first part of the study, researchers with University College London, the Medical Research Council and King’s College London Institute of Psychiatry analyzed ghrelin levels and other indicators of hunger from two groups of participants—those with the high obesity-risk FTO gene (AA group) and those with the low obesity-risk version (TT group)—who were perfectly matched for body weight, fat distribution and social factors such as education level. The results evidently showed that AA group participants not only reported feeling hungrier after a meal than their TT group counterparts, but had “much higher circulating ghrelin levels,” suggesting “that the obesity-risk variant (AA) group do not suppress ghrelin in a normal way after a meal.”

The second part of the study apparently relied on functional magnetic resonance imaging (fMRI) “to measure how the brain responds to pictures of high-calorie and low-calorie food images, and non-food items, before and after a meal.” In this scenario, those with the FTO gene variant “rated pictures of high-calorie foods as more appealing after a meal than the low-risk group,” and the fMRI “revealed that the brains of the two groups responded differently to food images (before and after a meal) and to circulating levels of ghrelin.” To explain these differences, researchers over-expressed the FTO gene in mouse and human cells “and found that this altered the chemical make-up of ghrelin mRNA (the template for the ghrelin protein) leading to higher levels of ghrelin itself.”

“What this study shows us is that individuals with two copies of the obesityrisk FTO variant are biologically programmed to eat more. Not only do these people have higher ghrelin levels and therefore feel hungrier, their brains respond differently to ghrelin and to pictures of food—it’s a double hit,” the lead author was quoted as saying. “At a therapeutic level this arms us with some important new insights to help in the fight against the obesity pandemic. For example, we know that ghrelin (and therefore hunger) can be reduced by exercise like running and cycling, or by eating a high-protein diet. There are also some drugs in the pipeline that suppress ghrelin, which might be particularly effective if they are targeted to patients with the obesity-risk variant of the FTO gene.”