High intake of palatable food predicts binge-eating independent of susceptibility to obesity: an animal model of lean vs obese binge-eating and obesity with and without binge-eating.
OBJECTIVE
To determine the stability of individual differences in non-nutritive 'junk' palatable food (PF) intake in rats; assess the relationship of these differences to binge-eating characteristics and susceptibility to obesity; and evaluate the practicality of using these differences to model binge-eating and obesity.


METHODS
Binge-eating prone (BEP) and resistant (BER) groups were identified. Differential responses to stress, hunger, macronutrient-varied PFs, a diet-induced obesity (DIO) regimen and daily vs intermittent access to a PF+chow diet, were assessed.


METHODS
One hundred and twenty female Sprague-Dawley rats.


METHODS
Reliability of intake patterns within rats; food intake and body weight after various challenges over acute (1, 2, 4 h), 24-h and 2-week periods.


RESULTS
Although BEP and BER rats did not differ in amount of chow consumed, BEPs consumed >50% more intermittent PF than BERs (P<0.001) and consistently so (alpha=0.86). BEPs suppressed chow but not PF intake when stressed, and ate as much when sated as when hungry. Conversely, BERs were more affected by stress and ate less PF, not chow, when stressed and were normally hyperphagic to energy deficit. BEP overeating generalized to other PFs varying in sucrose, fat and nutrition content. Half the rats in each group proved to be obesity prone after a no-choice high fat diet (DIO diet) but a continuous diet of PF+chow normalized the BEPs high drive for PF.


CONCLUSIONS
Greater intermittent intake of PF predicts binge-eating independent of susceptibility to weight gain. Daily fat consumption in a nutritious source (DIO-diet; analogous to a fatty meal) promoted overeating and weight gain but limiting fat to daily non-nutritive food (PF+chow; analogous to a snack with a low fat meal), did not. The data offer an animal model of lean and obese binge-eating, and obesity with and without binge-eating that can be used to identify the unique physiology of these groups and henceforth suggest more specifically targeted treatments for binge-eating and obesity.
Boggiano
M M
MM
Department of Psychology, Behavioral Neuroscience Division, University of Alabama at Birmingham, Birmingham, AL, USA. boggiano@uab.edu
Artiga
A I
AI
Pritchett
C E
CE
Chandler-Laney
P C
PC
Smith
M L
ML
Eldridge
A J
AJ
D000818:Animals; D002032:Bulimia; D004195:Disease Models, Animal; D005260:Female; D005523:Food Supply; D020022:Genetic Predisposition to Disease; D006815:Hunger / Q000502:physiology; D009042:Motivation; D009765:Obesity / Q000209:etiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013315:Stress, Psychological / Q000150:complications*