Binge eating is a form of compulsive food intake in which short-term homeostatic control of meal size is periodically and dramatically compromised. About 14 million people in the United States engage in binge eating. Binge relapse rates are high, treatment options are limited and the high co-morbidity with other disorders makes treatment a particular challenge. Understanding the factors that contribute to the transition from casual to compulsive binge-type consumption of food is critical for the development of new and effective treatment strategies. What accounts for the loss of control that occurs during these brief, but extremely large meals? Bingeing is characterized by the intermittent, excessive consumption of forbidden foods that are typically high in fat and sugar. Data from an animal model we have developed indicate that intermittent consumption, in-and-of itself, contributes to bingeing. While the effect of intermittency on palatable food intake has been well characterized in our model, the reason why intermittency enhances intake has not. Such information would have clinical relevance, since most people binge intermittently. We hypothesize that rats with intermittent access to optional palatable foods "learn to binge", and that this process involves an integrated neural network composed of forebrain targets of midbrain dopamine projections, as well as functional alterations in D1 and D2 receptor actions. Data collected over the past project period using our model support this scenario, and suggest that the behavior of our bingeing rats is more compulsive than that of control rats, and that the response to dopamine ligands, as well as the involvement of dopamine projection sites, differ between these groups. The results we have obtained map nicely onto findings reported in human subjects;therefore, we believe that our model provides a reasonable way to begin to clarify some of the factors that contribute to the development and maintenance of binge-type eating.
The Aims of the proposed research are to: 1) determine specific components of intermittent access that promote binge eating (cue predictability, binge experience, macronutrient composition of the food), 2) identify forebrain regions that are critical to the development of binge eating, and 3) determine the contributions of dopamine D1- and D2-like receptors to the binge intake. Binge eating is a form of compulsive food intake in which short-term homeostatic control of meal size is periodically and dramatically compromised. About 14 million people in the United States engage in binge eating. Binge relapse rates are high, treatment options are limited and the high co-morbidity with other disorders makes treatment a particular challenge. Understanding the factors that contribute to the transition from casual to compulsive binge-type consumption of food is critical for the development of new and effective treatment strategies.

Public Health Relevance

Binge eating is a form of compulsive food intake in which short-term homeostatic control of meal size is periodically and dramatically compromised. About 14 million people in the United States engage in binge eating. Binge relapse rates are high, treatment options are limited and the high co-morbidity with other disorders makes treatment a particular challenge. Understanding the factors that contribute to the transition from casual to compulsive binge-type consumption of food is critical for the development of new and effective treatment strategies.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Project (R01)
Project #
5R01MH067943-08
Application #
8270611
Study Section
Neurobiology of Motivated Behavior Study Section (NMB)
Program Officer
Rossi, Andrew
Project Start
2003-04-01
Project End
2014-03-31
Budget Start
2012-04-01
Budget End
2013-03-31
Support Year
8
Fiscal Year
2012
Total Cost
$340,352
Indirect Cost
$108,903
Name
Pennsylvania State University
Department
Nutrition
Type
Schools of Allied Health Profes
DUNS #
003403953
City
University Park
State
PA
Country
United States
Zip Code
16802
Wojnicki, Francis H E; Brown, Shane D; Corwin, Rebecca L W (2014) Factors affecting the ability of baclofen to reduce fat intake in rats. Behav Pharmacol 25:166-72
Wojnicki, F H E; Charny, G; Corwin, R L W (2013) Baclofen-induced reductions in optional food intake depend upon food composition. Appetite 64:62-70
Babbs, R K; Unger, E L; Corwin, R L W (2013) 2-Hydroxyestradiol enhances binge onset in female rats and reduces prefrontal cortical dopamine in male rats. Horm Behav 63:88-96
Wojnicki, F H E; Babbs, R K; Corwin, R L W (2013) Environments predicting intermittent shortening access reduce operant performance but not home cage binge size in rats. Physiol Behav 116-117:35-43
Yu, Zhiping; Geary, Nori; Corwin, Rebecca L (2011) Individual effects of estradiol and progesterone on food intake and body weight in ovariectomized binge rats. Physiol Behav 104:687-93
Babbs, R K; Wojnicki, F H E; Corwin, R L W (2011) Effect of 2-hydroxyestradiol on binge intake in rats. Physiol Behav 103:508-12
Corwin, Rebecca L W (2011) The face of uncertainty eats. Curr Drug Abuse Rev 4:174-81
Corwin, Rebecca L; Avena, Nicole M; Boggiano, Mary M (2011) Feeding and reward: perspectives from three rat models of binge eating. Physiol Behav 104:87-97
Wang, Y; Wilt, D C; Wojnicki, F H E et al. (2011) Fat emulsion composition alters intake and the effects of baclofen. Appetite 57:628-34
Wojnicki, F H E; Babbs, R K; Corwin, R L W (2010) Reinforcing efficacy of fat, as assessed by progressive ratio responding, depends upon availability not amount consumed. Physiol Behav 100:316-21

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