Oxytocin as feeding inhibitor: maintaining homeostasis in consummatory behavior

Abstract

Initial studies showed that the anorexigenic peptide oxytocin (OT) regulates gastric motility, responds to stomach distention and to elevated osmolality, and blocks consumption of toxic foods. Most recently, it has been proposed to act as a mediator of general and carbohydrate-specific satiety and regulator of body weight. In the current review, we discuss the function of OT as a homeostatic inhibitor of consumption, capable of mitigating multiple aspects of ingestive behavior and energy metabolism.

Copyright © 2010 Elsevier Inc. All rights reserved.

Figures

Fig. 1. Topography of central OT pathways involved in food intake regulation with special emphasis on functional significance of the circuits

OT neurons project from parvocellular PVN neurons in the hypothalamus to brainstem sites known to regulate feeding (NTS, AP, DMNV) and to the pituitary, where OT is released to the general circulation. While the brainstem-hypothalamus pathways have been extensively studied in relation to OT’s involvement in anorexigenic responses stemming from peripheral parameters, such as GI tract distension, osmolality of the blood, etc., many other feeding-related sites that contain OT terminals or OT receptors have not been comprehensively evaluated in relation to anorexigenic action of OT. These include areas involved in reward (ventral tegmental area, VTA; nucleus accumbens, NAc; bed nucleus of the stria terminalis, BST), affect (dorsal raphe nucleus, DR), energy homeostasis (ventromedial hypothalamic nucleus, VMH) and stress (amygdala, Amy; and parabrachial nucleus; PB) (Buijs et al. , 1983, De Vries and Buijs, 1983, Kirchgessner, Sclafani, 1988, Olson et al. , 1993).

Fig. 2. A schematic representation of functional relationship between OT neuronal activity/release and feeding-related behaviors, processes and physiological conditions