When supplemented into the diet, fermentable carbohydrates decrease appetite and prevent body weight gain in rodents and humans. The mechanisms by which fermentable carbohydrates regulate appetite are largely unknown. However, the metabolically active short-chain fatty acids (SCFAs), which are produced following microbial fermentation of non-digestible carbohydrates are thought to mediate the effects. As hypothalamic arcuate signalling is important for regulating food intake we hypothesised that the fermentable carbohydrate inulin exerts its satiating effects by altering neuronal activity within the arcuate nucleus. To allow voluntary oral administration we incorporated inulin into a palatable, gelatin-based matrix. As a measure of neuronal activation c-fos expression was measured at 4hours and 30minutes following consumption of either inulin or control. C-fos expression in the arcuate nucleus was increased 30% following inulin consumption. This may be due to release of gut hormones as previous studies demonstrate increased GLP-1 release by SCFAs, alternatively SCFAs may act via the vagus nerve or directly within the hypothalamus to alter arcuate activity. This data demonstrates that the mechanism by which fermentable carbohydrate decreases appetite involves altering neuronal activity within the arcuate nucleus.