Abstracts

Rationale: The ketogenic diet (KD) is a high-fat and low carbohydrate diet used as an alternative treatment for refractory epilepsy. However, it remains controversial whether the KD presents a protective effect against status epilepticus (SE). We investigated the neuroprotective and anticonvulsant effects of the ketogenic diet containing coconut oil on pilocarpine-induced SE model. Methods: Thirty-one young male Wistar rats were fed a control diet (7 % lipids) or a KD containing coconut oil (69.8 % lipids). The control and ketogenic diets had a lipid:carbohydrate+protein ratio of 3.5:1 and 1:11.8, respectively. All rats were subjected to lithium-pilocarpine SE (127 mg/kg; intraperitoneal (i.p) and 30 mg/kg; i.p, respectively) 30 days after the dietary treatment onset (CONTROL DIET+PILO, n=15; KETO+PILO, n=16). The latency, number, and severity of limbic seizures before and during (90 min) SE were analyzed by video recording. Neuronal loss in hippocampus was evaluated by Fluoro-Jade (FJ) and FJ positive neurons (FJ+) were counted 24 hours after SE. Unpaired Student’s t-test was used for comparative analysis and mean differences were considered statistically significant at p≤0.05 (GraphPad Prism 5.00, Inc. San Diego, CA, USA). Results: Rats fed a KD showed lesser weight gain (p < 0.05) but a higher feed efficiency (p < 0.0001) compared to the control diet. The concentration of β-hydroxybutyrate was significantly higher in the rats fed a KD (1,28±0,3M) compared to the control diet (0,70 ± 0,1M). There were no differences in the latency to SE or seizure features between CONTROL DIET+PILO and KETO+PILO groups. Rats in the KETO+PILO group had a lower number of FJ neurons in the hilus region of the hippocampus when compared with the CONTROL DIET+PILO group (p=0.009; n=6). On the other hand, the number of FJ neurons in CA1 and CA3 hippocampal subfields did not differ between the groups. Conclusions: Taken together, our data suggest that KD did not present an anticonvulsant effect in SE. However, the KD protects the hilar neurons during the acute phase of epileptogenic process Funding: FAPEAL; CAPES; CNPq; Federal University of Alagoas