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Objective: Obesity is associated with alterations in corticolimbic-striatal brain regions involved in food motivation and reward. Stress and the presence of food cues may each motivate eating and engage corticolimibic-striatal neurocircuitry. It is unknown how these factors interact to influence brain responses and whether these interactions are influenced by obesity, insulin levels, and insulin sensitivity. We hypothesized that obese individuals would show greater responses in corticolimbic-striatal neurocircuitry after exposure to stress and food cues and that brain activations would correlate with subjective food craving, insulin levels, and HOMA-IR.Research Design and Methods: Fasting insulin levels were assessed in obese and lean subjects who were exposed to individualized stress and favorite-food cues during functional MRI.Results: Obese, but not lean, individuals exhibited increased activation in striatal, insular, and hypothalamic regions during exposure to favorite-food and stress cues. In obese but not lean individuals, food craving, insulin, and HOMA-IR levels correlated positively with neural activity in corticolimbic-striatal brain regions during favorite-food and stress cues. The relationship between insulin resistance and food craving in obese individuals was mediated by activity in motivation-reward regions including the striatum, insula, and thalamus.Conclusions: These findings demonstrate that obese, but not lean, individuals exhibit increased corticolimbic-striatal activation in response to favorite-food and stress cues and that these brain responses mediate the relationship between HOMA-IR and food craving. Improving insulin sensitivity and in turn reducing corticolimbic-striatal reactivity to food cues and stress may diminish food craving and affect eating behavior in obesity. [ABSTRACT FROM AUTHOR]

The obesity epidemic has unfolded in a matter of decades, not millennia, and therefore cannot be attributed to a drift in the genome. Rather, the temporal characteristics of the epidemic more closely track environmental and lifestyle changes, such as reduced physical activity, increased availability of palatable and energy-dense foods and drinks, and increased acceptance of eating outside of meal time (among others). One important observation is that not everyone is becoming obese. This suggests that individual factors interact with recent environmental changes to predispose some to overeat. One hypothesis that has been gaining traction in the neuroscience community is that individual differences in the neural encoding of foods may predispose some to overeat in the presence of a surplus of energy-dense, palatable foods and drinks. The aim of this review is to highlight several possible ways by which individual differences in the neurophysiology of food reward may lead to overeating. [ABSTRACT FROM AUTHOR]