Figure 2.

Metabolic effects of OXT. OXT is produced in the paraventricular nucleus (PVN) and supraoptic nucleus (SON), shown in dark text. PVN and SON are sensitive to indicators of nutrient status, including nutrients themselves (eg, glucose, sucrose, leucine, fat-derived satiety factors) as well as other hormones (eg, leptin, insulin, GLP1, CCK, gastric afferents). Nuclei with OXT receptors (indicated by the Y shape) both within the hypothalamus and outside the hypothalamus respond to the presence of OXT and influence energy intake and energy balance. Hypothalamus and brainstem regulate the homeostatic drive to eat, and the brain reward network regulates the hedonic drive to eat. Oxytocin-producing neurons in the PVN also receive regulatory input from the central melanocortinergic signaling pathways that influence appetite. Hypothalamus and brainstem also impact energy expenditure, with the most consistent evidence in support of this occurring via increased sympathetic nervous system tone. The entire OXT signaling network also influences social function, which affects complex behaviors related to metabolism (eg, eating, voluntary physical activity, psychosocial stress). Oxytocin is also secreted into the periphery via the posterior pituitary, where it exerts metabolic effects in multiple organ systems (eg, GI motility, muscle and bone anabolism, lipolysis, pancreatic insulin secretion). Abbreviations: α-MSH, α-melanocyte stimulating hormone; ARC, arcuate nucleus; CCK, cholecystokinin; DMN, dorsomedial nucleus; GI, gastrointestinal; GLP1, glucagon-like peptide 1; MM, mammillary nuclei; NAc, nucleus accumbens; NTS, nucleus tractus solitarius; OXT, oxytocin; PVN, paraventricular nucleus; SNS, sympathetic nervous system; SON, supraoptic nucleus; VMN, ventromedial nucleus; VTA, ventral tegmental area.