Opioidergic consequences of dietary-induced binge eating

Abstract

Endogenous opioids are involved in the hedonic aspects of eating. Opioid impairments and alterations have been implicated in the pathophysiology of bulimia nervosa and binge eating disorder. Specific contributions by Bartley G. Hoebel have furthered the understanding how cyclical caloric restriction and intermittent optional access to sugar solutions results in opioid-like forebrain neural alterations and dependency in rodents. The present study sought to investigate caudal brainstem and nodose ganglion mu-opioid receptor mRNA alterations in a rodent model of dietary-induced binge eating of sweetened fat (vegetable shortening blended with 10% sucrose). Five groups (n = 7 or 8) of adult female Sprague Dawley rats were exposed to various dietary conditions for 6 weeks. As measured by in situ hybridization, there was reduced (approximately 25% from naive) mu-opioid receptor mRNA in the nucleus of the solitary tract (NTS) in the binge access group, which had intermittent calorie restriction and optional limited access to the sweetened fat. A similar reduction in expression was demonstrated in the continuous access group, which has unlimited optional sweetened fat and an obese phenotype. In the nodose ganglion, mu-opioid receptor mRNA was increased (approximately 30% from groups with sweetened fat access) in rats with intermittent caloric restriction alone. Our findings and the body of work from the Hoebel laboratory suggest that dietary-induced binge eating can consequentially alter opioidergic forebrain and hindbrain feeding-related neural pathways. Future work is needed to determine whether similar alterations are involved in the maintenance and progression of binge eating and other related eating pathologies.

Intermittent Feeding Schedules—Behavioural Consequences and Potential Clinical Significance

“…or in a 2 h period following restriction to induce bingeing [83]. µ opioid receptor knock out mice had similar intake to wild types on a restricted schedule but showed suppression of FAA prior to scheduled feeding [84].…”

Dietary conditions and highly palatable food access alter rat cannabinoid receptor expression and binding density

“…The protocol includes “binge access” period causes an overeating pattern of intake that is produced by imposing intermittent food restriction with limited access to a highly palatable food (i.e., sweetened fat; vegetable shortening blended with 10% sucrose) [41,42]. The purpose of the present investigation was to determine whether such patterns of overeating result in alterations in the CB1 receptor mRNA and binding density in neural structures involved in body weight regulation and food intake [8,9].…”

“…The purpose of the present investigation was to determine whether such patterns of overeating result in alterations in the CB1 receptor mRNA and binding density in neural structures involved in body weight regulation and food intake [8,9]. Analyses were performed on frozen tissue collected from animals used in a previously published study measured mu-opioid receptor mRNA in the hindbrain and nodose ganglion [42]. …”

Binge-Like Eating Attenuates Nisoxetine Feeding Suppression, Stress Activation, and Brain Norepinephrine Activity

“…We have previously used female rats in the restrict binge feeding schedule, which demonstrated a similar specific escalation in sweetened fat intake over time [30], [32]. As a result of the gender disparity in the prevalence of eating disorders, our current ongoing experiments utilize young female rats.…”