The Role of Lateral Hypothalamus Orexin Glucose-Inhibited Neurons in Binge-Eating Disorder
Abstract
Repeated patterns of intermittent calorie restriction followed by re-feeding of highly palatable foods can contribute to binge pathologies in some at risk populations. For this project we use a murine of model of dietary binge eating that investigates the interaction of intermittent calorie restriction (i.e., hypoglycemia bouts) and rapid consumption of highly palatable food (i.e., sweetened fat; SF) on lateral hypothalamus (LH) orexin neurons. Mice with repeated access to SF without the repeated calorie restriction do not demonstrate a binge phenotype. Behavioral data indicates that using chemogenetic activation of LH orexin neurons we determined that mice with SF access only developed a binge phenotype. In vitro electrophysiology experiments demonstrated intermittent calorie restriction increases glutamate transmission on LH orexin target dopamine-containing in the ventral tegmental area (VTA). This increased VTA glutamine current could be a mechanism to drive binge eating following repeated calorie restriction. Our research is designed to investigate how binge eating pathology is different from normal homeostatic eating, as it pertains to the addictive nature of highly palatable rewarding foods. Our goal is to assist in developing clinically effective treatment strategies for improving the quality of life for military service members and veterans afflicted with eating disorders.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2021
- Accession Number
- AD1152691
Entities
People
- Nicholas T. Bello
- Vanessa R. Routh
Organizations
- Rutgers University–New Brunswick