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Abstract
Binge eating episodes are characterized by uncontrollable, distressing eating of a large amount of highly palatable food and represent a central feature of bingeing related eating disorders. Research suggests that inflammation plays a role in the onset and maintenance of eating-related maladaptive behavior. Markers of inflammation can be selectively altered in discrete brain regions where they can directly or indirectly regulate food intake. In the present study, we measured expression levels of different components of cytokine systems (IL-1, IL-6, IL-18, TNF-α and IFN-ɣ) and related molecules (iNOS and COX2) in the preoptic and anterior-tuberal parts of the hypothalamus of a validated animal model of binge eating. In this animal model, based on the exposure to both food restriction and frustration stress, binge-like eating behavior for highly palatable food is not shown when animals are exposed to the frustration stress during the estrus phase. We found a characteristic down-regulation of the IL-18/IL-18 receptor system (with increased expression of the inhibitor of the pro-inflammatory cytokine IL-18, IL-18BP, together with a decreased expression of the binding chain of the IL-18 receptor) and a three-fold increase in the expression of iNOS specifically in the anterior-tuberal region of the hypothalamus of animals that develop a binge-like eating behavior. Differently, when food restricted animals were stressed during the estrus phase, IL-18 expression increased, while iNOS expression was not significantly affected. Considering the role of this region of the hypothalamus in controlling feeding related behavior, this can be relevant in eating disorders and obesity. Our data suggest that by targeting centrally selected inflammatory markers, we may prevent that disordered eating turns into a full blown eating disorder.
Highlights
Eating disorders are characterized by a persistent disturbance of eating and eating-related behavior that results in the altered consumption of food and significantly impairs physical health and/or psychosocial functioning [1]
3.1 Females rats with a history of food restrictions consumed more highly palatable food following exposure to an acute frustration stress when tested in non-estrus As in our previous studies [16], we found that while rats lost weight during the 4-day food restriction period they regained it during the subsequent 4-day ad libitum food period
The statistical analysis, which included the between-subjects factors of history of intermittent food restriction and stress during testing, and the estrus phase showed that palatable food intake was significantly affected by history of food restriction and stress [F(1, 32) = 39.9, p < 0.01], by estrus phase [F(1, 32) = 66.9, p < 0.01] with a significant interaction between the two factors [F(1, 32)= 11.02, p < 0.01]
Summary
Eating disorders are characterized by a persistent disturbance of eating and eating-related behavior that results in the altered consumption of food and significantly impairs physical health and/or psychosocial functioning [1]. Several brain areas (such as bed nucleus of the stria terminalis- BNST-,lateral habenula, or ventral tegmental area) are involved in regulating feeding, appetite, motivational behavior, and are sensitive to changes in cytokine systems [18, 19], here we have focused our attention on the hypothalamus This area represents the neuro-endocrine interface in the brain and it is a key station for central circuits to orchestrate the maintenance of body homeostasis or allostasis because of its high responsivity to immune signals. We evaluated changes in the transcription of inflammatory genes in both the anterior-tuberal and in the preoptic hypothalamus of animals exposed to cyclic food restrictions and frustration stress developing a binge-like eating behavior to look for the region specificity of the effects with respect to feeding and related behavior. The effect of the estrus phase was investigated in the same experimental conditions, given that food-restricted animals experiencing the frustration stress during estrus failed to develop binge-like eating behavior [23]
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