ESPE Abstracts (2018) 89 FC6.2

Impaired Brain Satiety Responses to a Meal in Children with Obesity

Christian Rotha, Susan Melhornb, Clinton Elfersa, Kelley Scholza, Mary Rosalynn De Leonb, Brian Saelensa & Ellen Schurb


aDepartment of Pediatrics, Seattle Children’s Research Institute, Seattle, Washington, USA; bDepartment of Medicine, General Internal Medicine, Seattle, Washington, USA


Behavioral studies suggest that brain satiety responses to food consumption are altered in children with obesity. We studied brain regions involved in satiety processing using functional magnetic resonance imaging (fMRI) before and after a test meal. Satiety-related hormonal changes were assessed. Fifty-four 9-11 year-old children with obesity (OB) and 22 children with healthy weight (HW) were studied. Subjects underwent two fMRI scans, one before and one after a test meal, and finally had an ad libitum buffet meal to test satiety. Serial blood samples and measures of subjective appetite were obtained. Neural activation for the contrast high-calorie food vs. objects and low-calorie foods vs objects was assessed in brain regions of an extended satiety network encompassing ventral and dorsal striatum, amygdala, ventral tegmental area/ substantia nigra, insula and medial orbitofrontal cortex. While subjective appetite scores of hunger and fullness changed similarly between groups around the test meal, marked differences in brain activation were noted between OB and HW children. Regarding the global average of brain activation within the extended satiety network, in HW children activation was significantly reduced from pre to post meal in response to viewing pictures of high calorie food pictures (P<0.01), while such change from pre to post meal was not seen in OB children, despite appropriate gut hormone (peptide YY, glucagon-like peptide-1, active ghrelin) responses to the test meal in both groups. The lack of central satiety response in OB children was associated with greater degree of insulin resistance. Even when reductions in post-prandial ghrelin were substantial, OB children demonstrated persistent post-prandial activation by high-calorie food cues. OB subjects consumed more total calories at the ad libitum buffet (1156±57 vs HW 803±64 kcal, P<0.001, unadjusted). In conclusion, HW children demonstrated physiological central satiety responses, i.e. reductions of neural activation by high-calorie food cues following a test meal in areas of the extended satiety network which was not present in OB children. Our data suggest that children with obesity exhibit an impaired central, as opposed to peripheral, satiety response, which may predispose them to overconsumption of calories or difficulty with weight loss. Clinicaltrials.gov #NCT02484976. Supported by NIH R01DK098466.

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