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Ketogenic diet is a high-fat, low-carbohydrate, and adequate-protein diet. It is well-established as a treatment option for drug-resistant childhood epilepsies. Our study aimed to evaluate Selenium levels and oxidative stress in children receiving ketogenic diet for intractable seizures for 6 months. This is a comparative case-control study included 90 children under 6 years age. They were subdivided into three groups. Group I: Thirty patients with drug-resistant epilepsy under antiepileptic drugs only. Group II: Thirty patients with drug-resistant epilepsy under treatment with ketogenic diet for 6 months and antiepileptic drugs. Group III: Thirty age and sex-matched healthy children as controls. Full history taking with special emphasis on severity and frequency of seizures, neurological examination, anthropometric measurements and laboratory analysis for serum Malonaldehyde, and total antioxidant capacity and Selenium were done for all participants. The frequency and severity of seizures were significantly lower in group II receiving ketogenic diet than group I on antiepileptic drugs only. Selenium levels were significantly lower in epileptic patients in comparison to controls. However, it was markedly lower in the ketogenic diet group. Malonaldehyde levels were significantly higher in epileptic children in comparison to controls, with lower values among ketogenic diet group when compared to patients on antiepileptic drugs only. Total antioxidant capacity levels were significantly lower in epileptic patients in comparison to controls, with higher values among ketogenic diet group as compared to epileptic patients on pharmacological treatment. Ketogenic diet is an effective treatment for refractory epilepsy for its anti-epileptic mechanism. It also may exert antioxidant effects. The nutrient content of the ketogenic diet may not meet the recommended daily allowance for selenium. So, this should be taken into consideration for supplementation of minerals in adequate amounts for patients receiving this diet.

Background Exercise benefits a variety of organ systems in mammals, and some of the best recognized effects of exercise on muscle are mediated by the transcriptional peroxisome proliferator-activated receptor gamma co-activator 1-α (PGC-1α). The regulatory effect of swimming on muscle PGC-1α, FNDC5 mRNA expression, and subsequently irisin levels is more controversial. This study aimed to investigate the role of swimming as an exercise on the expression of peroxisome proliferator-activated receptor-gamma coactivator1 alpha (PGC-1α) and Fibronectin type III domain containing 5 (FNDC5) mRNA in skeletal muscle and assessment of serum omentin, adropin, irisin, and PGC-1α levels in high carbohydrate high fat (HCHF) diet induced obesity in rats. Sixty male albino rats are randomly divided into 4 groups (15 rats/group). In the first group (control), rats are fed with standard diet. The 2nd group (cont + swim) is fed on standard diet and made swimming exercise. The 3rd group of rats is fed on HCHF, whereas in the 4th group (HCHF + swim) is also fed on HCHF diet and made swimming exercise for 20 weeks. Blood glucose, insulin, HOMA-IR, lipid profile, omentin, irisin, adropin, and PGC-1α were measured. Also, FNDC5 and PGC-1α are extracted and purified from muscle tissue samples measured by PCR test. Results Our results showed significant increase in glucose, insulin, insulin resistance, cholesterol, and triglycerides with significant decrease in omentin, irisin, adropin, PGC-1α, and HDL in HCHF group as compared to the control group. These results improved after exercise in all parameter in HCHF + swim group compare to HCHF group. Also, there was inverse correlation between omentin and fasting glucose and HOMA-IR in HCHF + swim group. Conclusions It concluded that swimming exercise improved all the above measured parameters in serum and tissues which might have been promising for the prevention of metabolic diseases.

AIM: The alteration in the gut microbial community has been regarded as one of the main factors related to obesity and metabolic disorders. To date, little is known about Moringa oleifera as a nutritional intervention to modulate the microbiota imbalance associated with obesity. Therefore we aim to explore the role of aqueous Moringa oleiferous leaf extract on Lactobacilli and Bifidobacteria in high-fat diet-induced obesity and to investigate whether any restoration in the number of caecal Lactobacilli and Bifidobacteria could modulate obesity-induced inflammation.METHODS: Young Swiss albino mice were divided into three groups according to their diet. Two of them were fed on either high fat diet or high fat diet+aqueous extract of Moringa oleifera leaf, while the third group was fed on the control diet. Bacterial DNAs were isolated from the mice digesta samples for bacteria level estimation using Quantitative real-time polymerase chain reaction along with serum interleukin-6 and lipid profileRESULTS: Compared to the normal control mice, high-fat diet feeding mice showed significantly reduced intestinal levels of Bifidobacteria, and increased body weight, interleukin 6, and levels of Lactobacilli. Upon treatment with Moringa oleifera, body weight, interleukin 6, and both bacteria levels were significantly restoredCONCLUSIONS: Our findings suggest that Moringa oliefera aqueous leaf extract may contribute towards the pathophysiological regulation of weight gain, inflammation associated with high-fat-induced-obesity through gut bacteria modulation.