EFFECTS OF OMEGA-3 FATTY ACIDS ASSOCIATED WITH ANTIOXIDANT VITAMINS IN OVERWEIGHT AND OBESE CHILDREN.

Introduction: Antioxidants and unsaturated fatty acids have protective effects in obesity. Aim: We investigated the benefits of Omega-3 fatty acids associated with antioxidant vitamins in obese children. Magnesemia and calcemia were observed in relation with other metabolic parameters, before and after the treatment. Materials and methods: 60 obese children were compared with 35 normal weight children. Each obese child received daily, one pill, containing: 130mg docosahexaenoic acid, 25mg of eicosapentaenoic acid, vitamin A 200µg, vitamin D 1,25µg, vitamin E 2,5mg and vitamin C 30mg for three months. All the participants were instructed not to change their lifestyle. Results: The serum values for these minerals and for 25(OH) vitamin D were lower in obese children. The obese children had insulin resistance (HOMA-IR) and an imbalance of serum adipocytokines. In obese children, the body mass index was negatively correlated with calcemia (r=-0.34) and serum 25(OH) vitamin D (r=-0.33). The HOMA-IR was negatively correlated with magnesemia (r=-0.34) and serum adiponectin (r=-0.29). The treatment improved the mineral serum level, the insulin sensitivity and the adipocytokines levels. Conclusion: In obese children, the intake of Omega-3 fatty acids associated with antioxidant vitamins, for three months improved calcemia and magnesemia and increased insulin sensitivity.

HEMATOLOGICAL INDICES RELATED TO VITAMIN D DEFICIENCY IN OBESE CHILDREN.

Introduction: Vitamin D is involved in differentiation and induction of erythropoiesis in bone marrow cells. Aim: We compared the serum 25(OH) vitamin D level in obese children versus control and found correlations between vitamin D level and hematological indices in obese children. Materials and methods: 25 overweight and obese patients and 15 normal weight children were enrolled in an observational study . Results: In obese children, the serum level of 25(OH) vitamin D was significantly (p<0.04) lower (20.60 ng/mL) compared with the value from normal weight ones (25.63 ng/mL) and the body fat percentage BFP was higher. We found a positive correlation (r=0.44, p<0.05) between serum vitamin D and hemoglobin level and a negative one between serum vitamin D and the number of platelets (r= -0.43, p<0.05). Also, the serum iron was at the lower normal limit in the obese children and negatively correlated with the percent of the body fat (r= -0,62, p<0.05). Conclusion: Obese children have vitamin D deficiency. The hemoglobin level and the number of platelets are correlated with the serum level of 25(OH) vitamin D. Supplements with vitamin D may have pleiotropic effects, including those on bone marrow activity.

MATERNAL-FETAL METABOLISM DISORDERS INDUCED BY MATERNAL OBESITY IN AN ANIMAL MODEL.

CONTEXT: Adipokines secreted by fat cells are vital to the control of energy metabolism, communicating the nutrient status with the tissues responsible for controlling both energy intake and expenditure and insulin sensitivity. OBJECTIVE: We aimed to prove in an experimental animal study that maternal obesity has long term adverse fetal metabolic consequences, which pass on even to the next generation of descendants. DESIGN: The effects of maternal obesity have been studied on animal model using 50 obese female Wistar rats, in which we induced obesity by high-calorie high-fat diet administered by gavage. SUBJECTS AND METHODS: Obese rat females were sacrificed at gestation term and we analyzed the secretion of adipokines from maternal venous blood: leptin and adiponectin, placental, pancreatic, liver and brain homogenates lipid peroxidation levels estimated by: MDA (malonyl-dialdehyde), total thiols and GSH - as antioxidant factors and routine biochemistry. RESULTS: Low levels of adiponectin and increased levels of leptin positively correlated with the value of placental and fetal tissue lipid peroxidation (from the liver, pancreas and brain) measured by elevated MDA and total thiols and low levels of GSH. The lipid peroxidation in the organs examined generated consistent results, showing high levels of peroxidation expressed through high values of MDA in the groups with Omega 6 supplements respectively no supplementation, and low levels of antioxidants expressed through glutathione and thiols. CONCLUSIONS: Endocrine secretion of adipokines from the adipocytes and the recruited macrophages of obese mothers is positively correlated with placental and tissue lipid peroxidation level and routine biochemical parameters.

The oxidative hypothesis of senescence.

The oxidative hypothesis of senescence, since its origin in 1956, has garnered significant evidence and growing support among scientists for the notion that free radicals play an important role in ageing, either as "damaging" molecules or as signaling molecules. Age-increasing oxidative injuries induced by free radicals, higher susceptibility to oxidative stress in short-lived organisms, genetic manipulations that alter both oxidative resistance and longevity and the anti-ageing effect of caloric restriction and intermittent fasting are a few examples of accepted scientific facts that support the oxidative theory of senescence. Though not completely understood due to the complex "network" of redox regulatory systems, the implication of oxidative stress in the ageing process is now well documented. Moreover, it is compatible with other current ageing theories (e.g, those implicating the mitochondrial damage/mitochondrial-lysosomal axis, stress-induced premature senescence, biological "garbage" accumulation, etc). This review is intended to summarize and critically discuss the redox mechanisms involved during the ageing process: sources of oxidant agents in ageing (mitochondrial -electron transport chain, nitric oxide synthase reaction- and non-mitochondrial- Fenton reaction, microsomal cytochrome P450 enzymes, peroxisomal beta -oxidation and respiratory burst of phagocytic cells), antioxidant changes in ageing (enzymatic- superoxide dismutase, glutathione-reductase, glutathion peroxidase, catalase- and non-enzymatic glutathione, ascorbate, urate, bilirubine, melatonin, tocopherols, carotenoids, ubiquinol), alteration of oxidative damage repairing mechanisms and the role of free radicals as signaling molecules in ageing.

[Biochemical changes in senile cataract]. / Modificari biochimice în cataracta senila.

Oxidative mechanism may play an important role in maturity onset cataract. But, nowadays, there is no answer whether cataract is the result of oxidation per se or of exaggerated and inappropriate physiological responses to oxidation. Also, senile cataract may be considered a conformational disease. Understanding the mechanisms of cataractogenesis will lead to a better therapy.