Changes in paraoxonase 1 (PON1) activities have been observed in a variety of diseases involving oxidative stress, such as CVD. However, its role in obesity has not been fully established. In the present study, we aimed (1) to genotype sixteen PON1 SNP, (2) to measure serum PON1 activities and (3) to correlate these findings with the incidence of childhood obesity and related traits. We conducted a case-control study of 189 normal-weight and 179 obese prepubertal children, and we measured four different PON1 activities: lactonase; paraoxonase; arylesterase; diazoxonase. Although none of these activities was significantly different between the obese and normal-weight children, lactonase activity was found to be positively correlated with HDL-cholesterol and ApoA1 levels and negatively correlated with myeloperoxidase and fatty acid-binding protein 4 levels. Among the sixteen genotyped PON1 SNP, only the intronic SNP rs854566 exhibited a significant association with obesity (OR 0·61, 95 % CI 0·41, 0·91; P¼ 0·016). This genetic variant was also associated with increased diazoxonase, lactonase and arylesterase activities and decreased paraoxonase activity. Other genetic variants exhibited different association patterns with serum activities based on their location within the PON1 gene, and SNP that were located within the promoter were strongly associated with lactonase, arylesterase and diazoxonase activities. The functional variant Q192R exhibited the greatest effect on paraoxonase activity (P¼5·88 £ 10 242). In conclusion, SNP rs854566 was negatively associated with childhood obesity and with increased serum PON1 activities in prepubertal children. We determined that lactonase is a reliable indicator of PON1 activities and should be included in future studies of PON1 function.

RSV induced OS in AB. An increase in GSSG correlated with the disease severity in the infants. OS may contribute to the pathogenesis of RSV-AB.

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Summary Childhood obesity is a costly burden in most regions with relevant and adverse long‐term health consequences in adult life. Several studies have associated excessive body weight with a specific profile of gut microbiota. Different factors related to fecal microorganism abundance seem to contribute to childhood obesity, such as gestational weight gain, perinatal diet, antibiotic administration to the mother and/or child, birth delivery, and feeding patterns, among others. This review reports and discusses diverse factors that affect the infant intestinal microbiota with putative or possible implications on the increase of the obesity childhood rates as well as microbiota shifts associated with excessive body weight in children.

Purpose: The aims of this study were; 1) to evaluate if there is an association between the serum levels of the novel insulin-like adipokine isthmin-1 (ISM1) and obesity-related phenotypes in a population of Spanish children, 2) to investigate the plausible molecular alterations behind the alteration of the serum levels of this protein in children with obesity. Methods: The study population is a sub-cohort of the PUBMEP research project, consisting of a cross-sectional population of 119 pubertal children with overweight (17 boys, 19 girls), obesity (20 boys, 25 girls) and normal weight (17 boys, 21 girls). All subjects were classified into experimental groups according to their sex, obesity and insulin resistance (IR) status. They counted on anthropometry, glucose, and lipid metabolism, inflammation and cardiovascular biomarkers as well as ISM1 serum levels measured. This population was intended as a discovery population in which to elucidate the relationship between obesity and ISM1 levels in children. Furthermore, the study population had blood whole-genome DNA methylation allowing deepening into the obesity-ISM1 molecular relationship. Results: Higher serum levels of ISM1 were observed in boys with obesity when compared with normal-weight (P=0.004), and overweight (P=0.007). ISM1 serum levels were positively associated with BMI Z-score (P=0.005), and negatively with myeloperoxidase (MPO) (p=0.043) in boys. Nevertheless, we did not find associations between ISM1 serum levels and metabolic outcomes in girls, indicating a putative sexual dimorphism. DNA methylation levels in two-enhancer-related CpG sites of ISM1 (cg03304641 and cg14269097) were associated with serum levels of ISM1 in children. Discussion: We report an unprecedented study that provides a major step forward showing that ISM1 is robustly associated with obesity in pubertal boys, elucidating how this protein might be of special relevance as a new biomarker of obesity in children.

Background/objectives: Puberty and obesity have been associated with vitamin D deficiency but there is a lack of studies assessing this triple relationship at once. Thus, the aim of this study was to evaluate, under a cross-sectional design, the relationship between sex hormone levels and serum 25-hydroxyvitamin D (25(OH)D), taking into account pubertal status and obesity degree. Subjects/methods: A total of 460 participants from the GENOBOX study (241 females), aged 6-18 years were included in the analysis. Children were divided in groups according to their pubertal stage (prepubertal (n = 225) and pubertal (n = 235)) and obesity degree (normal weight children (n = 100) and children with overweight/obesity (n = 360)). Serum 25(OH)D, Follicle-Stimulating Hormone (FSH) and Luteinizing hormone (LH), estradiol and testosterone were measured. 25(OH)D levels were categorized and the hormones concentration wasadjusted by sex and converted into tertiles. Mann Whitney and Kruskal-Wallis tests, and quantile regression were performed. Results: Pubertal children showed lower serum concentrations of 25(OH)D than prepubertal children (median: 20 ng/mL vs. 24 ng/mL, respectively; p = 0.006). Moreover, within normal weight children, differences were found for 25(OH)D levels according to tertiles of testosterone (I: 27 ng/mL; II: 30 ng/mL; III: 19 ng/ mL, p = 0.008). Among overweight/obese, differences were found according to