Binge-type eating in rats is facilitated by neuromedin U receptor 2 in the nucleus accumbens and ventral tegmental area

Ashley E. Smith, James M. Kasper, Ara Thirteen, Noelle C. Anastasio, Jonathan D. Hommel

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Binge-eating disorder (BED) is the most common eating disorder, characterized by rapid, recurrent overconsumption of highly palatable food in a short time frame. BED shares an overlapping behavioral phenotype with obesity, which is also linked to the overconsumption of highly palatable foods. The reinforcing properties of highly palatable foods are mediated by the nucleus accumbens (NAc) and the ventral tegmental area (VTA), which have been implicated in the overconsumption behavior observed in BED and obesity. A potential regulator of binge-type eating behavior is the G protein-coupled receptor neuromedin U receptor 2 (NMUR2). Previous research demonstrated that NMUR2 knockdown potentiates binge-type consumption of high-fat food. We correlated binge-type consumption across a spectrum of fat and carbohydrate mixtures with synaptosomal NMUR2 protein expression in the NAc and VTA of rats. Synaptosomal NMUR2 protein in the NAc demonstrated a strong positive correlation with binge intake of a “lower”-fat (higher carbohydrate) mixture, whereas synaptosomal NMUR2 protein in the VTA demonstrated a strong negative correlation with binge intake of an “extreme” high-fat (0% carbohydrate) mixture. Taken together, these data suggest that NMUR2 may differentially regulate binge-type eating within the NAc and the VTA.

Original languageEnglish (US)
Article number327
Issue number2
StatePublished - Feb 2019


  • BED
  • Binge-eating disorder
  • Binge-type eating
  • NMUR2
  • Neuromedin U receptor 2
  • Nucleus accumbens
  • Obesity
  • Ventral tegmental area

ASJC Scopus subject areas

  • Food Science
  • Nutrition and Dietetics


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