Obesity-linked genetic variant changes brain’s response to food cues


Genes and sensitivity to environmental cues both contribute to obesity, but the relationship between these two is not well understood. A recent paper published in PNAS shows that children who have a genetic predisposition for obesity have a different neurological response to food, as well as larger reward centers. These two findings suggest that at least some of the genetic predisposition for obesity works by altering brain structures that respond to food.

The study looked at children who have a genetic variant that’s been associated with obesity risk. People with this genetic variant tend to have a high body fat percentage and BMI. Scientists suspect that the gene also influences food intake and choices, but not exercise habits. Based on previous work, the researchers behind the new paper theorize that this gene influences brain functions.

The authors recruited 78 children between the ages of nine and 12 for their study. These participants were all screened for the obesity-related genetic variant. Nineteen of the participants were considered high-risk because they had two copies of the variant. Thirty-seven had only one copy, and 22 did not have it at all; both of these groups were considered low-risk. The children were all asked to watch-age appropriate television which was interrupted with both regular and food-related commercials.

While the participants were watching these videos, the researchers used functional MRI (fMRI) to measure the responsiveness of the brain’s reward center to the food commercials. Using an Analysis of Variance comparison technique (ANOVA), they found that the children with the obesity-linked genetic variation had significantly stronger activation of reward centers in the brain when they saw the food-related commercials. This was true even among normal weight children who had the obesity-linked variant.

The researchers did not see the same association when they looked at the difference between overweight children and normal-weight children independent of the gene variant. In other words, when the gene variant was not present, this test couldn’t distinguish between overweight children and normal-weight children. This finding suggests that increased activation of reward centers is only linked to the obesity gene and not to the actual weight or body fat percentage of the children.

Structural MRI showed that portions of the reward center of the brain were significantly larger in children with the obesity-linked genetic variant when compared to controls.

Taken together, this work shows an association between one genetic risk for obesity and heightened reward responses to food cues, as well as an enlargement of the reward center in the brain. This suggests that overeating might be an ongoing risk for healthy weight children who have this obesity-linked variant.

Nature Human Behavior, 2016. DOI: 10.1073/pnas.1605548113 (About DOIs)

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