Exploring the role of beta-endorphin in activity-based anorexia in mice.

Abstract

Anorexia nervosa (AN) remains one of the most lethal mental health disorders and is poorly understood from a neurobiological perspective. The most widely used animal model of AN is activity-based anorexia (ABA) where scheduled food presentation leads to a spontaneous maladaptive increase in running-wheel activity and rapid weight loss in rodents, recapitulating specific aspects of AN. Research using the ABA paradigm to probe the role of hedonic and homeostatic circuits has indicated that the hypothalamic proopiomelanocortin (POMC) system may play a role in both the increased activity and reduced food intake observed. Previous work has shown that Pomc mRNA and its peptide product beta-endorphin (β-end) are increased during the onset of ABA. β-end is reinforcing and increases locomotor activity, and mice lacking the mu opioid receptor (MOR), the primary target of β-end, display blunted food-anticipatory activity in the ABA paradigm. Thus, the current work was designed to determine if aspects of ABA would be diminished in mice lacking β-end. We did not find any significant differences in wheel-running, food intake, or body weight loss in β-end knockout mice of either sex during ABA compared to wild-type littermates. Therefore, we conclude that the development of ABA does not require β-end.