Two sources of medium-chain triglycerides--triheptanoin with anaplerotic properties and coconut oil with antioxidant features--have emerged as promising therapeutic options for the management of pharmacoresistant epilepsy. We investigated the effects of ketogenic diets (KDs) containing coconut oil, triheptanoin, or soybean oil on pilocarpine-induced status epilepticus (SE) in rats. Twenty-four adult male Wistar rats were divided into 4 groups and fed a control diet (7% lipids) or a KD containing soybean oil, coconut oil, or triheptanoin (69.8% lipids). The ketogenic and control diets had a lipid:carbohydrate + protein ratio of 1:11.8 and 3.5:1, respectively. SE was induced in all rats 20 days after initiation of the dietary treatment, through the administration of pilocarpine (340 mg/kg; i.p.). The latency, frequency, duration, and severity of seizures before and during SE were observed with a camcorder. SE was aborted after 3 h with the application of diazepam (5 mg/kg; i.p.). The rats in the triheptanoin-based KD group needed to undergo a higher number of seizures to develop SE, as compared to the control group (P< 0.05). Total weight gain, intake, energy intake, and feed efficiency coefficient, prior to induction of SE, differed between groups (P < 0.05), where the triheptanoin-based KD group showed less weight gain than all other groups, less energy intake than the Control group and intermediate values of feed efficiency coefficient between Control and other KDs groups. Triheptanoin-based KD may have a neuroprotective effect on the establishment of SE in Wistar rats.

This study evaluated the effects of a ketogenic diet (KD) based on extra virgin coconut oil (Cocos nucifera L., VCO), on the treatment of epileptic rats. Two sets of experiments were conducted. First, male Wistar rats underwent induction of status epilepticus (SE) with the administration of pilocarpine intraperitoneally 21 animals reached spontaneous recurrent seizures (SRS) and were randomly allocated to the dietary regimens and video-monitored for 19 days. In the second experiment, 24 animals were randomized immediately after the induction of SE and followed for 67 days. Diets were as follows: Control (AIN-93G; 7% lipid), KetoTAGsoya (KD based on soybean oil; 69.79% lipid), and KetoTAGcoco (KD based on VCO; 69.79% lipid). There were no differences in the latency to the first crisis, total frequency, and duration of the SRS between groups in 2 experiments. The data suggest no effects of KD, with or without VCO, in rats with pilocarpine-induced epilepsy.

SUMMARY OBJECTIVE Analyzing the association between ABI and the main risk factors for coronary artery disease in coronary patients. METHODS Were selected 156 adult patients from a hospital in Maceió, Alagoas. Were evaluated with risk factors age, obesity, hypertension, diabetes mellitus, smoking, and dyslipidemia. PAOD screening was performed by the ankle-brachial index (ABI). The Mann-Whitney, chi-square, and Fisher’s exact tests were used. Confidence Interval of 95% and a significance of 5%. RESULTS 67.3% (n=105) males, 52.6% (n=82) elderly, 23.1% (n = 34) obese, 72.4% 6% (n=113) hypertensive, 34.6% (n=54) diabetics, 53.2% (n=83) smokers, 34.6% (n=54) dyslipidemic and 70.5% (n=110) with a family history of CAD. 16.7% (n=26) of the individuals presented PAOD. Three factors were associated with PAOD: age group ≥ 60 years (OR:3.656; p=0.005), diabetes mellitus (OR:2.625; p=0.024) and hypertension (OR:5.528; p=0.008). No significant difference was observed in the variables smoking, dyslipidemia, family history of CAD, and obesity. CONCLUSION The independent risk factors for PAOD were age, diabetes mellitus, and systemic arterial hypertension.