The role of the opioid system in binge eating disorder

Giuliano, Chiara; Cottone, Pietro

doi:10.1017/s1092852915000668

Cited by 36 publications

(28 citation statements)

References 91 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results are consistent with previous observations, which show that pretreatment with naltrexone dose-dependently reduces binge eating in rats (Apfelbaum and Mandenoff, 1981; Blasio et al, 2014b). These effects are typically (Apfelbaum and Mandenoff, 1981; Rao et al, 2008), though not always (Blasio et al, 2014b), selective for highly palatable diets, and naltrexone is thought to exert its effects by reducing the hedonic properties of food (Giuliano and Cottone, 2015; Kelley et al, 2002; Le Merrer et al, 2009; Taha, 2010). Naltrexone and other opioid receptor antagonists have been investigated in clinical populations, with promising effects on reductions in food intake and hedonic responses to palatable food (de Zwaan and Mitchell, 1992; Ziauddeen et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

A behavioral and pharmacological characterization of palatable diet alternation in mice

Moore

Schlain

Mancino

et al. 2017

Pharmacology Biochemistry and Behavior

Self Cite

View full text Add to dashboard Cite

Obesity and eating disorders are widespread in Western societies. Both the increased availability of highly palatable foods and dieting are major risk factors contributing to the epidemic of disorders of feeding. The purpose of this study was to characterize an animal model of maladaptive feeding induced by intermittent access to a palatable diet alternation in mice. In this study, mice were either continuously provided with standard chow food (Chow/Chow), or provided with standard chow for 2 days and a high-sucrose, palatable food for 1 day (Chow/Palatable). Following stability of intake within the cycling paradigm, we then investigated the effects of several pharmacological treatments on excessive eating of palatable food: naltrexone, an opioid receptor antagonist, SR141716A, a cannabinoid-1 receptor antagonist/inverse agonist, and BD-1063, a sigma-1 receptor antagonist. Over successive cycles, Chow/Palatable mice showed an escalation of palatable food intake within the first hour of renewed access to palatable diet and displayed hypophagia upon its removal. Naltrexone, SR141716A, and BD-1063 all reduced overconsumption of palatable food during this first hour. Here we provide evidence of strong face and convergent validity in a palatable diet alternation model in mice, confirming multiple shared underlying mechanisms of pathological eating across species, and thus making it a useful therapeutic development tool.

show abstract

Section: Discussionmentioning

confidence: 99%

A behavioral and pharmacological characterization of palatable diet alternation in mice

Moore

Schlain

Mancino

et al. 2017

Pharmacology Biochemistry and Behavior

Self Cite

View full text Add to dashboard Cite

show abstract

“…Environmental food-associated stimuli, known as conditioned reinforcers, can robustly enhance the desire to eat even in absence of food per se or in absence of physiological needs (Everitt and Robbins, 2005;Robinson et al, 2015). With repeated pairings of a cue (conditioned stimulus) with food (unconditioned stimulus), the learned cue itself becomes salient (termed incentive salience), therefore triggering intense urges to obtain the associated reward, and also acts as a conditioned reinforcer able to maintain food seeking in the absence of food presentation (Giuliano et al, 2012;Velazquez-Sanchez et al, 2015;Giuliano and Cottone, 2015).…”

Section: Habitual Overeating Psychobehavioral Feature: Maladaptive Hamentioning

confidence: 99%

Pathological Overeating: Emerging Evidence for a Compulsivity Construct

Moore

Sabino

Koob

et al. 2016

Neuropsychopharmacol

Self Cite

100

View full text Add to dashboard Cite

Compulsive eating behavior is a transdiagnostic construct that is characteristic of medical and psychiatric conditions such as forms of obesity and eating disorders. Although feeding research is moving toward a better understanding of the proposed addictive properties of food, the components and the mechanisms contributing to compulsive eating are not yet clearly defined or understood. Current understanding highlights three elements of compulsive behavior as it applies to pathological overeating: (1) habitual overeating; (2) overeating to relieve a negative emotional state; and (3) overeating despite aversive consequences. These elements emerge through mechanisms involving pathological habit formation through an aberrant learning process, the emergence of a negative emotional state, and dysfunctions in behavioral control. Dysfunctions in systems within neurocircuitries that comprise the basal ganglia, the extended amygdala, and the prefrontal cortex result in compulsive eating behaviors. Here, we present evidence to relate compulsive eating behavior and addiction and to characterize their underlying neurobiological mechanisms. A major need to improve understanding of compulsive eating through the integration of complex motivational, emotional, and cognitive constructs is warranted.

show abstract

“…Neurochemical mechanisms of BE converge on activation of the mesocorticolimbic dopamine system(13, 14). Cue-induced craving correlates with BE in humans(15) and changes in extracellular dopamine in the dorsal striatum in response to food stimuli correlate with scores of BE severity in patients with BED(16).…”

Section: Introductionmentioning

confidence: 99%

Cytoplasmic FMR1-Interacting Protein 2 Is a Major Genetic Factor Underlying Binge Eating

Kirkpatrick

Goldberg

Yazdani

et al. 2017

Biological Psychiatry

Self Cite

147

View full text Add to dashboard Cite

Background Eating disorders are lethal and heritable; however, the underlying genetic factors are unknown. Binge eating is a highly heritable trait associated with eating disorders that is comorbid with mood and substance use disorders. Therefore, understanding its genetic basis will inform therapeutic development that could improve several comorbid neuropsychiatric conditions. Methods We assessed binge eating in closely related C57BL/6 mouse substrains and in an F2 cross to identify quantitative trait loci (QTL) associated with binge eating. We used gene targeting to validated candidate genetic factors. Finally, we used transcriptome analysis of the striatum via mRNA sequencing (RNA-seq) to identify the premorbid transcriptome and the binge-induced transcriptome to inform molecular mechanisms mediating binge eating susceptibility and establishment. Results C57BL/6NJ but not C57BL/6J mice showed rapid and robust escalation in palatable food consumption. We mapped a single genome-wide significant QTL on chromosome 11 (LOD=7.4) to a missense mutation in cytoplasmic FMR1-interacting protein 2 (Cyfip2). We validated Cyfip2 as a major genetic factor underlying binge eating in heterozygous knockout mice on a C57BL/6N background that showed reduced binge eating toward a wild-type C57BL/6J-like level. Transcriptome analysis of premorbid genetic risk identified the enrichment terms “morphine addiction” and “retrograde endocannabinoid signaling” whereas binge eating resulted in the downregulation of a gene set enriched for decreased myelination, oligodendrocyte differentiation, and expression. Conclusions We identified Cyfip2 as a major significant genetic factor underlying binge eating and provide a behavioral paradigm for future genome-wide association studies in populations with increased genetic complexity.

show abstract

The role of the opioid system in binge eating disorder

Cited by 36 publications

References 91 publications

A behavioral and pharmacological characterization of palatable diet alternation in mice

A behavioral and pharmacological characterization of palatable diet alternation in mice

Pathological Overeating: Emerging Evidence for a Compulsivity Construct

Cytoplasmic FMR1-Interacting Protein 2 Is a Major Genetic Factor Underlying Binge Eating

Contact Info

Product

Resources

About