Overconsumption of ultra-processed food and sedentary lifestyle are the main causes of obesity, which in turn, increases the risk of developing metabolic, cardiovascular, and psychiatric diseases. Loss of control over food intake and binge eating often worsen as obesity progresses. Many studies have shown the effect of obesity on gut-microbiota composition and inflammation. However, less is known about microbiota and central adaptations occurring during the initial phases of body weight gain. To address this question, we used a rat model of binge eating, in which, rats (C/P) were fed twice a week with homemade cheesecake, as palatable food, for two months. At the end of the feeding protocol, C/P rats developed cheesecake binge eating behavior compared to chow fed rats (C/C). Despite the lack of obesity and peripheral inflammation, C/P rats showed altered microbiota composition, increased Firmicutes/Bacteroidetes ratio (F/B ratio) and α-diversity. In the hypothalamus of C/P rats, using q-PCR, we observed impaired cytokine and leptin-signaling-related protein gene expression. Additionally, we performed immunofluorescence analysis of Iba1+ microglia cells in the hypothalamus consisting in microglia counting, branches analysis and fractal analysis. Cheesecake consumption in C/P rats led to increased number of Iba1+ cells and changes in their morphology. Microglia cells showed decreased complexity and increased density, known as typical features of a pro-inflammatory state. Taken together these data suggest that changes in microbiota composition and neuroinflammation precede obesity and could contribute to overeating. Therefore, strategies able to limit these gut-brain axis adaptations may be useful in preventing excessive body weight gain.