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Assessment of Binge-Like Eating Behavior in Mice Utilizing a Weekly Intermittent Access Paradigm

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Animal Models of Eating Disorders

Part of the book series: Neuromethods ((NM,volume 161))

Abstract

In humans, binge eating (BE) is central to the harmful effects of bulimia and binge eating disorder (BED). An estimated 30% of the obese population in the United States meets the diagnostic criteria for BED. Thus, BED is likely a major contributor to the current obesity epidemic. We developed a novel model to examine binge-like eating behavior in rodents that utilizes a schedule of 24-h weekly access to a highly palatable, nutritionally complete energy-dense diet (HED). This method for inducing BE has advantages over previous methods in that it does not require the use of exogenous stressors, caloric restriction, or entrained food anticipatory activity to induce the binge episode. Herein, we report that the BE response induced by this intermittent feeding paradigm can be maintained for at least 9 months in C57BL/6 mice. However, answers to a fundamental question remain. Can BE increase the risk of metabolic syndrome above and beyond the risk associated with obesity alone? Recent evidence in humans and rodents suggests that this may be the case. Given the high prevalence of BED in obesity, it is to be expected that there will be metabolic consequences of BE in this model and potentially in other BE models. However, the exact nature and if it is similar to that observed in frank obesity remains to be determined. We report on what is known about the metabolic consequences of long-term exposure to BE in mice with 24-h weekly access to an HED. While the changes we observed are subtle, over time they could have a significant impact on overall metabolism. Alterations in opioid receptor signaling pathways after repeated bingeing are discussed and may be one mechanism that links binge-like eating behavior with peripheral metabolism. Mice have particular advantages as a preclinical model mainly due to the sophisticated genetic techniques that are available in this species. Extensive characterization of the physiological, behavioral, and molecular changes associated with intermittent access to palatable diets will provide opportunities to identify and test novel therapeutic approaches to reduce BE and to understand its clinical translatability.

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Acknowledgments

This work was supported by the Klarman Family Foundation Grants Program in Eating Disorders Research (TAC) and the Mayo Clinic Foundation (PT, TAC). The authors would like to thank Allison E. Sahr for guidance with intermittent access models, Paulina Smith for technical support, and the Mayo Clinic in Arizona Mouse Metabolic Phenotyping Laboratory.

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Authors and Affiliations

  1. Metabolic HEALth Program, Scottsdale, AZ, USA

    Tiffany Tang, Natalie Barker, James Krantz, Alysia Polito, Petr Telensky & Traci A. Czyzyk

  2. Recursion Pharmaceuticals, Salt Lake City, UT, USA

    Michael A. Statnick

  3. Department of Physiology, Mayo Clinic Arizona, Scottsdale, AZ, USA

    Traci A. Czyzyk

Authors
  1. Tiffany Tang
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  2. Natalie Barker
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  3. James Krantz
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  4. Alysia Polito
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  5. Petr Telensky
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  6. Michael A. Statnick
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  7. Traci A. Czyzyk
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Correspondence to Traci A. Czyzyk .

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Editors and Affiliations

  1. Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA

    Nicole M. Avena

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Tang, T. et al. (2021). Assessment of Binge-Like Eating Behavior in Mice Utilizing a Weekly Intermittent Access Paradigm. In: Avena, N.M. (eds) Animal Models of Eating Disorders. Neuromethods, vol 161. Humana, New York, NY. https://doi.org/10.1007/978-1-0716-0924-8_4

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  • DOI: https://doi.org/10.1007/978-1-0716-0924-8_4

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  • Publisher Name: Humana, New York, NY

  • Print ISBN: 978-1-0716-0923-1

  • Online ISBN: 978-1-0716-0924-8

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