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 region 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-\uf061
and IFN-&3) 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 IL18, 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