Correction of compulsive overeating in rats after maternal deprivation in early age using a new antagonist of OX1 receptors

Abstract

Background. Compulsive overeating (bulimia nervosa, binge eating disorder) is the basis of eating disorders and is included in ICD-11 and DSM-5 as a manifestation of a non-chemical form of addiction. It is a behavioral disorder of impulsivity and compulsivity. Obesity and eating disorders are characterized by compulsive food consumption, similar to the compulsive drug use of substance use disorders.
 Aim. Study of the effect of the OX1 receptor antagonist anthorex on compulsive overeating in animals in a model of maternal deprivation.
 Materials and methods. Sexually mature male rats, which were separated from their mother for 3 hours after birth from days 2 to 12, were fed a high-carbohydrate diet every third day for 1 hour for 45 days. In this case, high-calorie food was placed within 5 cm of reach with visual contact 15 minutes before feeding. Orexin receptor antagonist Anthorex was administered intranasally for 7 days at a dose of 1 µg/1 µl, 20 µl.
 Results. Intermittent consumption of high-calorie foods caused compulsive overeating in rats. Sexually mature animals that experienced deprivation from their mother in early ontogenesis showed increased signs of compulsive overeating of high-carbohydrate foods in our model relative to the control (p 0.001). At the same time, the consumption of standard briquetted feed did not change. Intranasal administration of the OX1 receptor antagonist anthorex reduced the manifestations of compulsive overeating in rats after weaning under conditions of intermittent consumption of high-calorie food compared to the control group (p 0.05). Consumption of standard food did not differ relative to the control group, both before and after the course of administration of the orexin antagonist.
 Conclusion. The work suggest new ways of studying and synthesizing peptide drugs based on orexin and its antagonists for the correction of compulsive overeating caused by chronic stress in ontogenesis.