Binge eating in rats produced by combining dieting with stress.

This unit describes a rodent model of binge eating based on cyclic restriction, refeeding, footshock, and intermittent access to palatable food. These conditions mimic dieting, stress, and "junk" food indulgence, respectively, all common etiological and maintenance factors in human binge eating. Four groups of rats are used: one subjected to cyclic food restriction, another to acute footshock stress, another to both of these (R + S), and a control. Neither cyclic restriction nor stress alone produces binge eating, but the R + S rats, despite satiety, double their intake of palatable food in a discrete period of time (i.e., binge) when stressed. This protocol recapitulates critical properties of human binge eating, namely preference for palatable food, dieting- and stress-induced vulnerability to binging, and eating for reward versus metabolic need. This protocol permits study of the psychobiological underpinnings of binge eating and possibly also of addiction, impulsivity, and depression, which are co-morbid with binge eating.

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

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.

Stress and hunger alter the anorectic efficacy of fluoxetine in binge-eating rats with a history of caloric restriction.

OBJECTIVE: We examined the effect of fluoxetine to suppress binge eating in rats with a history of caloric restriction (CR) and the extent to which this effect was altered by stress and hunger. METHOD: To detect heightened sensitivity to fluoxetine, young female rats were used to determine a subthreshold anorectic dose (2 mg/kg, intraperitonally). Another group of rats was either fed ad libitum or given multiple CR (to 90% body weight) and refeeding-to-satiety cycles. One half of the rats were then either spared or subjected to foot shock stress before fluoxetine treatment. RESULTS: A history of CR alone produced bingelike eating on palatable food (p < .001) and, although stress did not affect intake, it rendered CR rats hypersensitive to the satiety effect of fluoxetine. The feeding-suppression was mainly for chow (p < .05) and the effect was abolished if the rats were in negative energy balance. DISCUSSION: Results support the utility of this animal model to elucidate serotonergic changes linking dieting to binge eating. The diverse effects of fluoxetine on the type of food, and in hungry versus sated rats, suggest alternate brain mechanisms should be concomitantly targeted for improved treatment of binge eating disorders.

Jejunal administration of linoleic acid increases activity of neurons in the paraventricular nucleus of the hypothalamus.

The present experiment examined whether neurons located in the paraventricular nucleus of the hypothalamus (PVN) respond to intestinal infusions of long-chain fatty acids. Single-unit recordings were made of neurons located in and adjacent to the PVN during jejunal administration of linoleic acid. Jejunal administration of linoleic acid increased single-unit activity of neurons located in the PVN but did not affect activity of neurons located in adjacent tissue outside the PVN. The largest increases in neuronal activity were observed in the anterior PVN (0.9-1.3 mm posterior to bregma) compared with the posterior PVN (1.8-2.1 mm posterior to bregma). Jejunal administration of saline failed to affect activity of neurons located either inside or outside the PVN. When the same neurons were subsequently tested for their response to intravenous administration of 2 microg/kg of CCK-8, excitatory responses were more frequently observed than inhibitory responses, but both types of responses were observed regardless of whether neurons were located inside or outside the PVN. In addition, there was no strong correlation between the magnitude of the neuronal response evoked by jejunal administration of linoleic acid compared with intravenous CCK-8. These data suggest that neurons located in the anterior PVN may play a role in the mediation of suppression of food intake produced by intestinal administration of lipids.

The role of palatable food and hunger as trigger factors in an animal model of stress induced binge eating.

OBJECTIVE: Dieting and stress are etiological factors in eating disorders, and dieting strongly predicts stress-induced overeating in the nonclinical population. We developed an animal model of binge eating in sated rats that is evoked by stress, but only in rats with a history of caloric restriction and only if highly palatable food (HPF) is available after stress. This study investigated the effect of known binge triggers, a taste of HPF and of hunger, on this type of binge eating. METHOD: Female rats were cycled through the R/S protocol but this time were given just a taste of HPF with ad lib regular chow. After another R/S cycle, rats were stressed during restriction (while hungry) and were given HPF and chow. RESULTS: Although binge eating did not occur if only chow was available after stress, just a taste of HPF sufficed to increase chow intake to more than 160% (p < 0.001) of rats with a history of restriction only, stress-only, or neither. Hunger increased the proportion of chow consumed by both restricted groups, but stress magnified this hunger-induced overeating by increasing HPF intake to 137% of restriction-only rats (p < 0.001). DISCUSSION: These effects suggest that binge eating in this model is motivated by reward, not metabolic need, and parallels observations of binge triggers described in clinical binge-eating disorders. This strengthens the validity of using this animal model to target the physiology and treatment of eating disorders preceded by dieting and stress.

Incidence of chaotic eating behaviors in binge-eating disorder: contributing factors.

Because dieting is not as common in patients with binge-eating disorder (BED) as among patients with bulimia or anorexia nervosa, the authors assessed the incidence, frequency, and contributing factors of semistarvation-like eating patterns in BED patients in this study, the first to explore such behaviors in a clinical population. They administered the Semistarvation-Associated Behaviors Scale (SSABS) to 54 women seeking BED treatment and to 29 controls. The aberrant eating behaviors among BED clients were associated with current dieting and certain BED criteria, (p < .05). The strongest contributor to chaotic eating patterns was negative affect preceding BED (r = .45, p < .001). This finding highlights the behavioral psychopathology of BED and strengthens the role of negative affect in precipitating binge episodes associated with the disorder. These behaviors may help maintain BED by creating a binge-negative affect cycle. The SSABS is a tool that may help break this cycle.