Abstract
The hypothalamic neurohormone oxytocin decreases food intake via largely unexplored mechanisms. We investigated the central nervous mediation of oxytocin’s hypophagic effect in comparison to its impact on the processing of generalized rewards. Fifteen fasted normal-weight, young men received intranasal oxytocin (24 IU) or placebo before functional magnetic resonance imaging (fMRI) measurements of brain activity during exposure to food stimuli and a monetary incentive delay task (MID). Subsequently, ad-libitum breakfast intake was assessed. Oxytocin compared to placebo increased activity in the ventromedial prefrontal cortex, supplementary motor area, anterior cingulate, and ventrolateral prefrontal cortices in response to high- vs. low-calorie food images in the fasted state, and reduced calorie intake by 12%. During anticipation of monetary rewards, oxytocin compared to placebo augmented striatal, orbitofrontal and insular activity without altering MID performance. We conclude that during the anticipation of generalized rewards, oxytocin stimulates dopaminergic reward-processing circuits. In contrast, oxytocin restrains food intake by enhancing the activity of brain regions that exert cognitive control, while concomitantly increasing the activity of structures that process food reward value. This pattern points towards a specific role of oxytocin in the regulation of eating behaviour in humans that might be of relevance for potential clinical applications.
Highlights
Oxytocin is produced in the paraventricular nucleus of the hypothalamus and released into the circulation via the posterior pituitary; in addition it is secreted directly into limbic, hind- and midbrain regions[1]
Analyses distinguishing between the responses to highand low-calorie food pictures indicated that when subjects were fasted, oxytocin compared to placebo increased activity in response to high- vs. low-calorie food items in the ventromedial prefrontal cortex (vmPFC), supplementary motor area (SMA), anterior cingulate cortex (ACC), and bilateral ventrolateral prefrontal cortex (vlPFC; all region of interest (ROI) analyses, p < 0.05, FWE-corrected at cluster and peak level; Fig. 2 and Table 2)
Our study in healthy men indicates that the brain mechanisms underlying the inhibitory effect of oxytocin on food intake can be differentiated from mediators of oxytocin-induced changes in the processing of generalized, monetary rewards
Summary
Oxytocin is produced in the paraventricular nucleus of the hypothalamus and released into the circulation via the posterior pituitary; in addition it is secreted directly into limbic, hind- and midbrain regions[1]. Food intake increases oxytocin secretion from the pituitary[20], and the peptide acts as a downstream mediator of the anorexigenic effect of the adipocyte leptin by sensitizing caudal brain stem nuclei to satiety signals like cholecystokinin[21,22,23]. Respective experiments in humans available so far[9,11,13] suggest that oxytocin decreases food intake in part by acting on reward-processing neuronal circuits It is unclear whether the contribution of oxytocin to the regulation of human eating behaviour is established via food-specific effects on distinct brain networks or, rather, is a by-product of oxytocin’s involvement in general reward processing; our study was performed to address this question. We expected to identify eating-related brain mechanisms that mediate the hypophagic effect of oxytocin, but differ from those that establish oxytocin’s role in the processing of generalized (monetary) rewards
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