Orbitofrontal cortex volume and brain reward response in obesity.

Abstract

Background/ObjectivesWhat drives overconsumption of food is poorly understood. Alterations in brain structure and function could contribute to increased food seeking. Recently brain orbitofrontal cortex volume has been implicated in dysregulated eating but little is know how brain structure relates to function.Subjects/MethodsWe examined obese (n=18, age=28.7.4±8.3 years) and healthy control women (n=24, age=27.4±6.3 years) using a multimodal brain imaging approach. We applied magnetic resonance and diffusion tensor imaging to study brain gray and white matter volume as well as white matter integrity, and tested whether orbitofrontal cortex volume predicts brain reward circuitry activation in a taste reinforcement-learning paradigm that has been associated with dopamine function.ResultsObese individuals displayed lower gray and associated white matter volumes (p<.05 family wise error (FWE)-small volume corrected) compared to controls in the orbitofrontal cortex, striatum, and insula. White matter integrity was reduced in obese individuals in fiber tracts including the external capsule, corona radiata, sagittal stratum, and the uncinate, inferior fronto-occipital, and inferior longitudinal fasciculi. Gray matter volume of the gyrus rectus at the medial edge of the orbitofrontal cortex predicted functional taste reward-learning response in frontal cortex, insula, basal ganglia, amygdala, hypothalamus and anterior cingulate cortex in control but not obese individuals.ConclusionsThis study indicates a strong association between medial orbitofrontal cortex volume and taste reinforcement-learning activation in the brain in control but not in obese women. Lower brain volumes in the orbitofrontal cortex and other brain regions associated with taste reward function as well as lower integrity of connecting pathways in obesity may support a more widespread disruption of reward pathways. The medial orbitofrontal cortex is an important structure in the termination of food intake and disturbances in this and related structures could contribute to overconsumption of food in obesity.