Combined dieting and stress evoke exaggerated responses to opioids in binge-eating rats.

Abstract

The authors developed an animal model of binge eating where history of caloric restriction with footshock stress (R + S) causes rats to consume twice the normal amount of palatable food. The authors tested the hypothesis that binge eating is mediated by changes in opioid control of feeding by comparing rats' anorectic and orexigenic responses to naloxone and butorphanol, respectively, and by testing the ability of butorphanol to elicit binge eating of chow when palatable food was absent. Mu/kappa opioid-receptor blockade and activation had exaggerated responses in the R + S rats with naloxone suppressing binge eating to control levels, and although butorphanol did not trigger chow binge eating, it enhanced binge eating of palatable food. These responses in sated normal-weight rats strengthen evidence that reward, over metabolic need, drives binge eating.

Baclofen, raclopride, and naltrexone differentially reduce solid fat emulsion intake under limited access conditions

“…Studies have shown mu-opioid antagonism reduces short-term intake of high-fat food as well as corn oil (Islam and Bodnar, 1990;Mizushiege et al, 2006). In a binge protocol in which combination foot-shock stress and dietary restriction induce binge-eating, mu-opioid antagonism suppressed binge consumption of a high-fat food (Boggiano et al, 2005). In addition, at least one study has shown a greater potency for the fat intake reducing effects of mu-opioid blockade relative to carbohydrate intake reducing effects, when the foods being compared were both highly palatable (chocolate vs. sugar-coated cereal) and equally preferred (Hagan et al, 1997).…”

A history of caloric restriction induces neurochemical and behavioral changes in rats consistent with models of depression

“…Recent work with an animal model of stress-induced binge-eating has led to initial discoveries of the mechanisms that underlie binge-eating including 5-HT and opioid dysregulation (Boggiano, et al, 2005;. Besides the availability of PF, this rat binge-eating model is based on a history of caloric restriction (HCR) with recovery of body weight and food intake to that maintained by never-restricted rats, which is more typical of human dieting that commonly antecedes eating disorders.…”

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

“…18,[27][28][29][30][31] Binge-eating is also associated with heightened reward sensitivity, which may enhance drive for PF. 10,32 Less is known regarding whether a high drive for PF predisposes the development of maladaptive eating habits and obesity. Although we cannot model in animals all of the many factors that contribute to individual food preferences in humans, we can identify rats with that overconsume PF and determine whether this contributes to obesity and binge-eating or behaviors consistent with binge-eating characteristics in humans.…”

“…Intermittent intake of PF alone promotes subsequent binge-like eating; 1,2 it also interacts with caloric restriction 3 and stress 4,5 to produce binge-eating; [6][7][8] and it changes central reward substrates 9,10 in ways similar to that caused by drugs of abuse. 2,11,12 It is also well known that palatable junk food contributes to passive overeating, weight gain and obesity in humans.…”