Bogdana Virgolici

Obese Childhood Dyslipidemia Management Beyond Statins — MUFA, PUFA, and Sea-buckthorn Supplements

The dyslipidemia pattern usually associated with childhood obesity consists of a combination of elevated triglyceridemia, decreased plasma high density lipoprotein cholesterol concentration and LDL-c concentration at the upper limit of the normal range. This type of dyslipidemia is associated with dense and small LDL, which are proatherogenic. High circulating levels of oxidized LDL were described in extreme pediatric obesity, in children with high fructose intake and are associated with insulin resistance. The worst effect on blood lipids have trans and saturated fatty acids. But the amount of total energy intake plays more important role in lipid profiles. In childhood obesity it seems that insulin resistance precedes the development of the metabolic syndrome feature and insulin resistance is correlated with dyslipidemia. Insulin resistance increases free fatty acid flux to the liver by decreased inhibition of lipolysis and also by increased de novo lipogenesis. Fish oil is rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and has hypotriglyceridemic effect in comparison to monounsaturated fatty acids. Passive in utero exposure to a hyperli‐ pidemic environment may have programmed these children for accelerated athero‐ sclerosis. The infant formula should be enriched with long chain fatty acids because this supplementation is associated with lower blood pressure during later childhood. In obese children, supplements with Omega-3 polyunsaturated fatty acids improve lipid profile, blood pressure values and inflammatory markers. Omega-3 fatty acids prevent metabolic syndrome, by reducing hepatic steatosis, visceral fat, by reducing serum triglycerides and improving insulin sensitivity. Potentially all compounds of

The role of adipose tissue as endocrine organ in the metabolic programming of fetuses derived from obese mothers

We aim to present the endocrine and paracrine role of the cytokines secreted by hypertrophied maternal fat cells on fetal and later on neonatal metabolic profile. The study used an animal model in order to analyze the influence of maternal adipokines secretion of fetal metabolism. We selected 50 female Wistar rats weighing between 200-250 g (normal weight 100-150g) to whom we induced obesity by high-fat, high-calorie food intake (80% of diet saturated fatty acids) and tracked the correlation of maternal adipokines secretion with placental and fetal lipid peroxidation level. The low adiponectin and increased leptin values as adipokines secreted by adipocytes of obese mothers were correlated with the level of placental and fetal tissue lipid peroxidation (from the liver, pancreas, brain), measured by elevated malonyldialdehyde and total thiols and the decreased levels of glutathione. It has been known for decades that fat tissue is not inert, but a true endocrine organ, which responds by secreting adipokines to different energy and hormonal stimuli. Endocrine secretion of adipokines from the adipocytes of obese mothers is positively correlated with placental and fetal lipid peroxidation levels. Fetal metabolic programming as an inducible phenomenon is explained partly by the influence of excess secretion of maternal adipokines.

Sea Buckthorn Pulp Oil Treatment Prevents Atherosclerosis in Obese Children

This study aimed to determine the effects of sea buckthorn pulp oil treatment (800 mg/day for 60 days) on inflammatory, systemic oxidative/reductive status and endothelial function, in obese children. A total of 41 obese children (10–18 years old) and thirty controls were enrolled. The measurements were done before and after pulp oil administration. Ultrasounds were used for flow-mediated dilatation (FMD) and carotid artery intima-media thickness (IMT) measurements and colorimetric and ELISA methods for biochemical parameters. In the obese children versus the lean ones, increased oxidative stress (high malonyldialdehyde, high respiratory burst (RB)), low antioxidant defence (low blood glutathione, low TEAC), inflammatory status (high CRP, ceruloplasmin), adipocytokines disturbance (low adiponectin and high leptin), insulin resistance (high fasting C peptide), low FMD (), and high IMT () were measured. Treatment reduced total cholesterol (), triglycerides (), RB (), leptin (), ceruloplasmin (), fasting C peptide (), blood pressure (), and IMT (). In conclusion, sea buckthorn pulp oil treatment prevents atherosclerosis by lowering triglyceridemia, cholesterolemia, and blood pressure (strong effects) and by reducing oxidative stress, inflammation, and insulin resistance (weak effects).