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Physiol Behav. 2013 Feb 17;110-111:122-8. doi: 10.1016/j.physbeh.2013.01.002. Epub 2013 Jan 10.

Differences in the neuronal response to food in obesity-resistant as compared to obesity-prone individuals.

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Division of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 80045, USA.


Despite living in an obesogenic environment, some individuals maintain a thin phenotype compared to the majority who are at risk for weight gain and obesity. Understanding how these different phenotypes regulate energy intake is critical. The objective of this study was to examine the differences in neuronal response to visual food cues in adults recruited as either obesity-resistant (OR) or obesity-prone (OP) based on self-identification, BMI, and personal/family weight history. 25 OR and 28 OP individuals were studied after 4 days of eucaloric energy intake. Functional magnetic resonance imaging (fMRI) was performed in the fasted and acute fed states (30 min after a test meal) while subjects viewed images of foods of high hedonic value and neutral non-food objects. Measures of appetite using visual analog scales were performed before and every 30 min after the test meal for 3 h. In the fasted state, food as compared to nonfood images elicited significant response in the insula, somatosensory cortex, parietal cortex, and visual cortex in both OR and OP. The acute fed state resulted in significant attenuation of these and other brain areas in the OR but not OP individuals. Furthermore, OP as compared to OR individuals showed greater activation of medial and anterior prefrontal cortex (PFC) in response to the test meal. Adjusting for fat mass did not impact these results. Attenuation of insula/PFC response to food images in the fed state was associated with greater reductions in hunger. These findings suggest that individuals prone to weight gain and obesity have altered neuronal responses to food cues in brain regions known to be important in energy intake regulation. These altered responses may represent an important mechanism contributing to excess energy intake and risk for obesity.

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