Pharmacological Interventions for Binge Eating: Lessons from Animal Models, Current Treatments, and Future Directions

Berner, Laura A.; Bocarsly, Miriam E.; Hoebel, Bartley G.; Avena, Nicole M.

doi:10.2174/138161211795656774

Cited by 38 publications

(34 citation statements)

References 101 publications

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“…Thus, it can provide a useful tool with which to study brain mechanisms associated with repeated binge-like bouts, and perhaps assist with the development of pharmacotherapies aimed at suppressing binge eating of, or perhaps “addiction” to, palatable food [26]. Such therapies might prove to be particularly useful among clinical populations expressing comorbid substance use and binge eating disorders [5, 6].…”

Section: The Sugar Addiction Modelmentioning

confidence: 99%

Feeding and reward: Perspectives from three rat models of binge eating

Corwin

Avena

Boggiano

2011

Physiology & Behavior

262

187

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Research has focused on understanding how overeating can affect brain reward mechanisms and subsequent behaviors, both preclinically and in clinical research settings. This work is partly driven by the need to uncover the etiology and possible treatments for the ongoing obesity epidemic. However, overeating, or non-homeostatic feeding behavior, can occur independent of obesity. Isolating the variable of overeating from the consequence of increased body weight is of great utility, as it is well known that increased body weight or obesity can impart its own deleterious effects on physiology, neural processes, and behavior. In this review, we present data from three selected animal models of normal-weight non-homeostatic feeding behavior that have been significantly influenced by Bart Hoebel’s 40+-yr career studying motivation, feeding, reinforcement, and the neural mechanisms that participate in the regulation of these processes. First, a model of sugar bingeing is described (Avena/Hoebel), in which animals with repeated, intermittent access to a sugar solution develop behaviors and brain changes that are similar to the effects of some drugs of abuse, serving as the first animal model of food addiction. Second, another model is described (Boggiano) in which a history of dieting and stress can perpetuate further binge eating of palatable and non-palatable food. In addition, a model (Boggiano) is described that allows animals to be classified as having a binge-prone vs. binge-resistant phenotype. Lastly, a limited access model is described (Corwin) in which non-food deprived rats with sporadic limited access to a high-fat food develop binge-type behaviors. These models are considered within the context of their effects on brain reward systems, including dopamine, the opioids, cholinergic systems, serotonin, and GABA. Collectively, the data derived from the use of these models clearly show that behavioral and neuronal consequences of bingeing on a palatable food, even when at a normal body weight, are different from those that result from simply consuming the palatable food in a non-binge manner. These findings may be important in understanding how overeating can influence behavior and brain chemistry.

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Section: The Sugar Addiction Modelmentioning

confidence: 99%

Feeding and reward: Perspectives from three rat models of binge eating

Corwin

Avena

Boggiano

2011

Physiology & Behavior

262

187

View full text Add to dashboard Cite

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“…These topics has been reviewed elsewhere (Kelley et al, 2002; Berner et al, 2011; Mercer and Holder, 1997; Nathan and Bullmore, 2009). Another set of clinical implications comes from a perhaps unexpected domain, sleep biology.…”

Section: New Directionsmentioning

confidence: 99%

Principles of motivation revealed by the diverse functions of neuropharmacological and neuroanatomical substrates underlying feeding behavior

Baldo

Pratt

Will

et al. 2013

Neuroscience & Biobehavioral Reviews

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Circuits that participate in specific subcomponents of feeding (e.g., gustatory perception, peripheral feedback relevant to satiety and energy balance, reward coding, etc.) are found at all levels of the neural axis. Further complexity is conferred by the wide variety of feeding-modulatory neurotransmitters and neuropeptides that act within these circuits. An ongoing challenge has been to refine the understanding of the functional specificity of these neurotransmitters and circuits, and there have been exciting advances in recent years. We focus here on foundational work of Dr. Ann Kelley that identified distinguishable actions of striatal opioid peptide modulation and dopamine transmission in subcomponents of reward processing. We also discuss her work in overlaying these neuropharmacological effects upon anatomical pathways that link the telencephalon (cortex and basal ganglia) with feeding-control circuits in the hypothalamus. Using these seminal contributions as a starting point, we will discuss new findings that expand our understanding of (1) the specific, differentiable motivational processes that are governed by central dopamine and opioid transmission, (2) the manner in which other striatal neuromodulators, specifically acetylcholine, endocannabinoids and adenosine, modulate these motivational processes (including via interactions with opioid systems), and (3) the organization of the cortical-subcortical network that subserves opioid-driven feeding. The findings discussed here strengthen the view that incentive-motivational properties of food are coded by substrates and neural circuits that are distinguishable from those that mediate the acute hedonic experience of food reward. Striatal opioid transmission modulates reward processing by engaging frontotemporal circuits, possibly via a hypothalamic-thalamic axis, that ultimately impinges upon hypothalamic modules dedicated to autonomic function and motor pattern control. We will conclude by discussing implications for understanding disorders of “non-homeostatic” feeding.

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“…The endocannabinoid system represents a promising target for the development of novel pharmacological agents that reduce food intake (Di Marzo, 2008; Kirkham, 2009; Berner et al , 2011; DiPatrizio and Piomelli, 2012; Mendez-Diaz et al , 2012). Antagonism of the type-1 cannabinoid (CB 1 ) receptor has been demonstrated to be a successful pharmacological approach for overeating and obesity.…”

Section: Introductionmentioning

confidence: 99%

Characterization of a shortened model of diet alternation in female rats

Blasio

Rice

Sabino

et al. 2014

Behavioural Pharmacology

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The prevalence of eating disorders and obesity in Western societies is epidemic and increasing in severity. Preclinical research focused on the development of animal models which can mimic the maladaptive patterns of food intake observed in certain forms of eating disorders and obesity. This study was aimed at characterizing a recently established model of palatable diet alternation in female rats. For this purpose, females rats were fed either continuously with a regular chow diet (Chow/Chow) or intermittently with a regular chow diet for 2 days and a palatable, high-sucrose diet for 1 day (Chow/Palatable). Following diet cycling, rats were administered rimonabant (0, 0.3, 1, 3 mg/kg i.p.) during access to either palatable diet or chow diet and were assessed for food intake and body weight. Finally, rats were pretreated with rimonabant (0 – 3 mg/kg, i.p.) and tested in the elevated plus maze during withdrawal from the palatable diet. Female rats with alternating access to palatable food cycled their intake, overeating during access to the palatable diet, and under-eating upon returning to the regular chow diet. Rimonabant treatment resulted in increased chow hypophagia and anxiety-like behavior in Chow/Palatable rats. No effect of drug treatment was observed on the compulsive eating of palatable food in the diet cycled rats. The results of this study suggest that withdrawal from alternating access to the palatable diet makes individuals vulnerable to the anxiogenic effects of rimonabant and provide etiological factors potentially responsible for the emergence of severe psychiatric side-effects following rimonabant treatment in obese patients.

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Pharmacological Interventions for Binge Eating: Lessons from Animal Models, Current Treatments, and Future Directions

Cited by 38 publications

References 101 publications

Feeding and reward: Perspectives from three rat models of binge eating

Feeding and reward: Perspectives from three rat models of binge eating

Principles of motivation revealed by the diverse functions of neuropharmacological and neuroanatomical substrates underlying feeding behavior

Characterization of a shortened model of diet alternation in female rats

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