Visceral adiposity and insular networks: associations with food craving

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Abstract
Accumulation of visceral adiposity can disrupt the brain’s sensitivity to interoceptive feedback, which is coded in the insula. This study aimed to test the link between visceral fat and the functional connectivity of two insulae regions relevant for eating behavior: the middle-dorsal insula (mIns), which codes homeostatic changes, and the rostral insula (rIns), which codes stable representations of food properties. We also assessed the impact of visceral adiposity-associated insulae networks on food craving. Seventy-five adults ranging in weight status (normal and excess weight) underwent resting-state functional magnetic resonance imaging (fMRI) and subjective food craving measures. We examined the association between visceral fat and seed-based functional connectivity of the mIns and the rIns, controlling for BMI, age, and sex, using multiple regressions in SPM8. We also tested if visceral fat mediated the association between insulae connectivity and food craving. Higher visceral adiposity was associated with decreased connectivity between the mIns and a cluster involving the hypothalamus and the bed nucleus of the stria terminalis. Decreased connectivity in this network was associated with greater food craving, a relation mediated by visceral adiposity. Visceral adiposity was also associated with increased connectivity between the mIns and the middle frontal gyri and the right intraparietal cortex, and between the rIns and the right amygdala. Accumulation of visceral adiposity is linked to disrupted functional connectivity within the mIns and rIns networks. Furthermore, the link between the mIns network and food craving is mediated by visceral fat. Findings suggest that visceral fat disrupts insula coding of bodily homeostatic signals, which may boost externally driven food cravings.

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