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1 Acta Neurobiologiae Experimentalis

1 2013

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The effects of ketogenic and calorie restricted diets on epileptic seizure in rats with mechanical brain injury

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Osoba J. , Setkowicz-Janeczko Z. , Gzielo-Jurek K. , Kielbinski M.

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Traumatic brain injury (TBI) is a major cause of mortality and morbidity in children and young adults. It initiates multiple cascades of events that lead to acute metabolic dysfunction and cellular energy crisis. TBI remains one of the most common and important causes of acquired epilepsy nowadays. The ketogenic diet (KD) is a specialized high-fat low-protein and low-carbohydrate diet which mimics the anticonvulsive effects of fasting, which were known to suppress seizures. KD is used primarily in children with seizures refractory to standard anticonvulsive drugs (AEDs). Many studies on the anticonvulsant effects of a KD have been performed. Unfortunately, the mechanism of action of the ketogenic diet remains unclear. Although the ketogenic diet is the best dietary therapy for epilepsy, there are other possible approaches including overall restriction of caloric intake. Dietary restriction seems a promising alternative to classic ketogenic diet, possibly because it is associated with higher levels of ketone bodies, which are themselves neuroprotective. Caloric restriction (CR) is defined as a decrease in energy intake without lowering nutritional value. CR improves behavioral outcomes after ischemic brain injury in rats and could possibly act as a neuroprotective factor in global ischemia. It has been also shown that chronic administration of CR may provide protection in the event of TBI. The aim of this research was to study the changes in susceptibility to pilocarpine-induced epileptic seizures in rats with mechanical brain injury. In 30-day-old male Wistar rats (P30), mechanical brain injury was performed. Immediately after, the calorically unrestricted ketogenic diet (KD) and calorically restricted standard laboratory rat chow diet (CR) were introduced. In order to check how the ketogenic diet and caloric restriction alone influence the epileptic seizure susceptibility, two groups of 30-day-old rats were fed KD and CR untill postnatal day 60. At that time, seizures were induced by pilocarpine injection. During the following 6-h period, the animals were continuously observed and motor seizures intensity were rated on a 6-point scale. We have found that KD, both alone or administered to animals with history of experimental brain injury, significantly increases the maximum intensity of pilocarpine-induced seizures, compared to CR fed healthy and injured controls, respectively. Surprisingly, KD and CR seem to have opposite effects in healthy animals as well as animals with a history of experimental brain injury. We have found that KD increases the maximum intensity of pilocarpine-induced seizures, compared to both calorically restricted and unrestricted normal diets. CR, on the other hand, decreases the seizure-genic effect of pilocarpine. This results in a continuum in which calorically restricted animals exhibit the weakest, and KD-fed animals the strongest seizures. To our knowledge, the effects of calorically-restricted and ketogenic diets on pilocarpine-induced seizures have not been previously studied. In other well established models of epilepsy, KD either attenuates or has little effect on seizure intensity.