The association between inflammation and the induction of seizures is well-known. It has been reported that non-alcoholic fatty liver disease (NAFLD) is associated with a pro-inflammatory state, and systemic inflammation may trigger central nervous system inflammation. This study aims to identify the impact of inflammation in a rat model of fatty liver on the propensity and severity of pentylenetetrazol (PTZ)-induced seizures. Twenty-four male Sprague-Dawley rats were divided into four groups. Groups 1 and 2 were administered a 35 % fructose solution over 8 weeks to induce the development of fatty liver while Groups 3 and 4 were fed normally as controls. Groups 1 and 3 were given 70 mg/kg PTZ, determining Racine Convulsion Scores (RCS) and onset times of the first myoclonic jerks (FMJ). Groups 2 and 4 were administered 35 mg/kg of PTZ, then EEG recordings were obtained to evaluate spike percentages. TNF-α levels in brain and liver tissues were also measured. While RCS's of fatty liver rats were higher than the control group (p > 0.05) as well as spike percentages (p < 0.05), FMJ onset time was significantly shorter. TNF-α levels in liver and brain tissues of the rats with NAFLD were significantly higher than the control rats. We found that rats with NAFLD demonstrated decreased seizure thresholds, possibly due to increased cytokine levels systemically and within the central nervous system. As such, epilepsy patients taking medications that may predispose the development of NAFLD must be carefully managed to prevent the possibility of increased seizure episodes.