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Sea Buckthorn Pulp Oil Treatment Prevents Atherosclerosis in Obese Children

DOI: 10.1155/2013/164941

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Abstract:

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). 1. Introduction According to research, the number of children who are clinically obese has raised threefold in the past 30 years [1]. The increase in prevalence and severity of obesity in children is concerning, as is progression to type 2 diabetes and cardiovascular diseases in adulthood [2]. Obesity is associated with chronic low-grade inflammation and insulin resistance [3]. In obesity, high plasma levels of leptin, TNF-α, IL-6, and other proinflammatory adipocytokines, together with increased plasma concentrations of fatty acids, mediate insulin resistance. Inflammatory pathways to insulin resistance include several serine/threonine kinases members and oxidative stress [4, 5]. Leptin seems to promote atherogenesis by stimulating vascular smooth muscle hypertrophy, inflammation, and oxidative stress [6]. But what happens with leptin in obese children has remained unknown [7]. While leptin is considered a biomarker of vascular dysfunction, adiponectin improves endothelial cells function. Adiponectin may protect the endothelium, via its insulin-sensitizing, antiatherogenic, anti-inflammatory, and antioxidant properties [8]. Recent studies on childhood obesity and adiponectin have demonstrated the contribution of hypoadiponectinemia to low-grade systemic chronic

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