Obesity Is Associated with Oxidative Stress Markers and Antioxidant Enzyme Activity in Mexican Children.

The relationship between metabolic disorders and oxidative stress is still controversial in the child population. The present cross-sectional study aimed to analyze the associations between obesity, cardiometabolic traits, serum level of carbonylated proteins (CPs), malondialdehyde (MDA), and the enzyme activity of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in children from Mexico City (normal weight: 120; obesity: 81). Obesity resulted in being positively associated with CAT (ß = 0.05 ± 0.01, p = 5.0 × 10-3) and GPx (ß = 0.13 ± 0.01, p = 3.7 × 10-19) enzyme activity. A significant interaction between obesity and sex was observed in MDA and SOD enzymatic activity (PMDA = 0.03; PSOD = 0.04). The associations between obesity, MDA level, and SOD enzyme activity were only significant in boys (boys: PMDA = 3.0 × 10-3; PSOD = 7.0 × 10-3; girls: p ≥ 0.79). In both children with normal weight and those with obesity, CP levels were positively associated with SOD enzyme activity (PNormal-weight = 2.2 × 10-3; PObesity = 0.03). In conclusion, in Mexican children, obesity is positively associated with CAT and GPx enzyme activity, and its associations with MDA levels and SOD enzyme activity are sex-specific. Therefore, CP level is positively related to SOD enzyme activity independently of body weight.

YAAM: Yeast Amino Acid Modifications Database.

Database URL: http://yaam.ifc.unam.mx/.

Nicotinamide prevents sweet beverage-induced hepatic steatosis in rats by regulating the G6PD, NADPH/NADP+ and GSH/GSSG ratios and reducing oxidative and inflammatory stress.

The disruption of redox state homeostasis, the overexpression of lipogenic transcription factors and enzymes, and the increase in lipogenic precursors induced by sweetened beverages are determinants of the development of nonalcoholic fatty liver disease. This study evaluated the action of nicotinamide (NAM) on the expression of glucose-6-phosphate dehydrogenase (G6PD) and redox, oxidative, and inflammatory states in a model of nonalcoholic hepatic steatosis induced by high and chronic consumption of carbohydrates. Male rats were provided drinking water with 30% glucose or fructose ad libitum for 12 weeks. Additionally, 30 days after the beginning of carbohydrate administration, some rats were simultaneously provided water with 0.06% or 0.12% NAM for 5h daily over the next 8 weeks. Biochemical profiles and expression levels of G6PD, tumor necrosis factor α (TNFα), and NADPH oxidase 4 (NOX4) were evaluated together with glutathione/glutathione disulfide (GSH/GSSG) and reduced nicotinamide adenine dinucleotide (phosphate)/nicotinamide adenine dinucleotide (phosphate) [NAD(P)H/NAD(P)] ratios and thiobarbituric acid reactive substances (TBARS). The results showed that hepatic steatosis induced by the chronic consumption of glucose or fructose was associated with body weight gain and increased levels of serum glucose, insulin, triacylglycerols, free fatty acids, transaminases, and TBARS. In the liver, the expression and activity of G6PD increased along with the GSSG, TBARS, and TG concentrations. These alterations were reduced by NAM treatment through the attenuation of increases in G6PD expression and activity and in the NADPH/NADP+ ratio, thereby slowing liver steatosis. NAM prevents redox, oxidative, and inflammatory alterations induced by high carbohydrate consumption.