Abstract
Elevated proinflammatory cytokines were reported in binge eating spectrum disorders characterized by intermittent overconsumption during periods of otherwise normal or restricted food intake. It is unknown whether binge eating promotes neuroinflammation, similar to that observed following chronic overconsumption of a high fat diet (HFD) in rodents. Here, we used a rodent model of binge-like eating to test the hypothesis that intermittent overconsumption of HFD promotes microglial reactivity in brain areas that control food intake. To promote overconsumption, one group of rats received chow plus intermittent access to HFD (INT). Control groups received either chow only (CHOW) or chow plus continuous access to HFD (CONT). Following behavioral testing, brains were processed to visualize ionized calcium-binding adaptor molecule 1 (Iba1), a microglial marker. INT rats consumed more calories than the control rats on days when the HFD was available, and fewer calories than the control rats on days when they only had access to chow. Despite consuming fewer total calories and 50% fewer fat calories, lean INT rats developed a pattern of microglial reactivity in feeding-relevant brain areas similar to obese CONT rats. We conclude that intermittent overconsumption of HFD, without diet-induced weight gain, promotes microglial reactivity in brain regions that control feeding.
Published Version
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