Abstract
The neuropeptide oxytocin is produced in the paraventricular hypothalamic nucleus and the supraoptic nucleus of the hypothalamus. In addition to its extensively studied influence on social behavior and reproductive function, central oxytocin signaling potently reduces food intake in both humans and animal models and has potential therapeutic use for obesity treatment. In this review, we highlight rodent model research that illuminates various neural, behavioral, and signaling mechanisms through which oxytocin’s anorexigenic effects occur. The research supports a framework through which oxytocin reduces food intake via amplification of within-meal physiological satiation signals rather than by altering between-meal interoceptive hunger and satiety states. We also emphasize the distributed neural sites of action for oxytocin’s effects on food intake and review evidence supporting the notion that central oxytocin is communicated throughout the brain, at least in part, through humoral-like volume transmission. Finally, we highlight mechanisms through which oxytocin interacts with various energy balance-associated neuropeptide and endocrine systems (e.g., agouti-related peptide, melanin-concentrating hormone, leptin), as well as the behavioral mechanisms through which oxytocin inhibits food intake, including effects on nutrient-specific ingestion, meal size control, food reward-motivated responses, and competing motivations.
Highlights
Oxytocin is a nine-amino-acid neuropeptide produced in the paraventricular hypothalamic nucleus (PVH) and supraoptic nucleus of the hypothalamus (SON) that acts on the G-protein coupled oxytocin receptors to impact several behaviors, including social behavior, reproduction, and lactation [1,2,3]
While central infusion of a glucagon-like peptide 1 (GLP-1) receptor antagonist followed by anorexigenic dose of oxytocin eliminated the anorexigenic effect of oxytocin, central infusion of an oxytocin receptor antagonist followed by synthetic GLP-1 ligand does not affect GLP-1induced anorexia [134]. Together these results suggest that oxytocin modulates hindbrain GLP-1 neuron signaling to inhibit food intake and that GLP-1-mediated activation of PVH neurons likely acts through non-oxytocinergic pathways to control food intake
The collective literature indicates that a primary mechanism through which oxytocin reduces food intake is to boost satiation signals to terminate an ongoing meal via hindbrain oxytocin receptor (OT-R) signaling
Summary
Oxytocin is a nine-amino-acid neuropeptide produced in the paraventricular hypothalamic nucleus (PVH) and supraoptic nucleus of the hypothalamus (SON) that acts on the G-protein coupled oxytocin receptors to impact several behaviors, including social behavior, reproduction, and lactation [1,2,3]. Pharmacological injection of oxytocin into the brain reduces food intake whereas administration of an oxytocin receptor antagonist has the opposite effect in rodents [4,5,6,7,8,9,10,11,12,13]. Collective evidence suggests that oxytocinergic regulation of eating behavior is important for satiation and meal size control rather than modulating interoceptive hunger and satiety state. We discuss known neural sites of action, oxytocin’s interactions with various other feeding-related peptides in the control of food intake, and volume transmission as a possible neural signaling pathway through which oxytocin influences eating behavior. We further review evidence related to behavioral mechanisms through which oxytocin inhibits food intake, including effects on satiation control, brain reward signaling pathways, and competing motivations
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