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  1. M. A. Cornier,
  2. S. S. Von Kaenel,
  3. J. R. Tregellas
  1. University of Colorado Health Sciences Center, Denver, CO


Certain individuals appear to be resistant to weight gain in an obesigenic environment, yet the mechanisms for this adaptation are unclear. These individuals may sense positive energy balance more appropriately leading to changes in intake. Preliminary studies have shown that thin individuals are very sensitive to overfeeding with significant changes in eating behaviors as compared to reduced-obese individuals. Sixteen thin ‘obese-resistant’ individuals (9 women and 7 men) and eight reduced-obese (RO) individuals (4 women and 4 men) were studied on two occasions in a randomized crossover design. Functional magnetic resonance imaging (fMRI) was performed in the morning after an overnight fast following 2 days of eucaloric feeding and following 2 days of overfeeding by 30% over basal needs. fMRI was performed with visual stimuli of three different categories: objects (O), utilitarian foods (U), and hedonic foods (H). BOLD echo-planar data (TR = 2000, TE = 30, 642 matrix, 240 mm2 FOV, 28 axial slices angled parallel to the planum sphenoidale, 4 mm thick, 0 mm gap, 3 T) were motion corrected, normalized to standard space, spatially smoothed, and assessed using the general linear model in SPM2. In the eucaloric state, visual stimuli of U as compared to O (U > O) resulted in greater activation of insula and inferior temporal visual cortex in RO as compared to thin individuals, while H > U resulted in frontal cortex activation in RO but not thin individuals. Overfeeding resulted in attenuation of visual and parietal cortex in both groups but also resulted in activation of posterior cingulate cortex in RO individuals and hypothalamic ‘deactivation’ in thin individuals (H > U). In summary, there appears to be a phenotypic difference in the neuronal activation in response to external food-related cues. Overfeeding appears to have a greater impact on neural structures important in processing of emotions in RO individuals while having a greater impact on neural structures involved with the homeostatic regulation of food intake in thin individuals.

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