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Introduction: Eating behavior is often established during the first years of life. Therefore, it is important to make a research on it to understand the relationships that children have with food and how this can contribute to prevent the development of childhood obesity. An appropriate assessment of eating behavior can be achieved using the "Child Eating Behavior Questionnaire" (CEBQ). This questionnaire has been validated in several populations and languages, but it has never been translated, adapted, and validated for Spanish children. Aim: To evaluate the reliability and internal consistency of the CEBQ questionnaire, culturally adapted and translated into Spanish (Spain), in Spanish families with children aged 3 to 6 years, as well as its association with children's body mass index (BMI) to test its construct validity. Materials and Methods: Children between 3 and 6 years old were recruited from the ongoing MELI-POP randomized controlled clinical trial, as well as from public schools located in middle class neighborhoods of Zaragoza, Spain, to complete the sample. Sociodemographic characteristics and anthropometric measures were obtained according to standardized methods. The 35-item CEBQ questionnaire was completed twice with a time difference of 3 weeks between each response. Statistical analyses included the evaluation of internal consistency and reliability of the questionnaire, a confirmatory factor analysis, and the association between the different CEBQ scales and the children's BMI. Results: A total of 197 children completed variables; 97 of them were boys (49.2%) and 100 girls (50.8%). Mean age of the total sample was 4.7 ± 0.9 years. There was a high test-re-test reliability of the questionnaire with values close to 1, with an average of 0.66 and a good internal consistency (Cronbach alpha with values above 0.7), so that a high reliability is established between the items in each scale. A gradual positive association was found between the score of different "pro-intake" scales of the CEBQ: "Food Responsiveness," "Emotional Overeating," and "Enjoyment of food" and the children's BMI; at the opposite, negative associations were observed between BMI and the score of anti-intake scales "Satiety Responsiveness," "Slowness in Eating," and "Emotional Undereating." Conclusion: The Spanish version of the CEBQ is a useful tool to assess the eating behavior of Spanish children because the high reliability and internal validity. There is a significant association between eating behavior and BMI in Spanish children. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. 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. 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 the tertiles of FSH (I: 25 ng/mL; II: 21 ng/mL; III: 19 ng/mL, p = 0.010), LH (I: 24 ng/mL; II: 21 ng/mL; III: 20 ng/mL, p = 0.004) and estradiol (I: 24 ng/mL; II: 21 ng/mL; III: 19.5 ng/mL, p = 0.043). Finally, higher concentrations of FSH were associated with a reduction of 25(OH)D levels in children with overweight/obesity (coefficient: −1.092, p = 0.022). Higher concentrations of sex hormones (FSH, LH, and estradiol) were associated with lower 25(OH)D levels in children with overweight or obesity. Thus, pubertal status and obesity degree need to be considered to achieve an optimal status of vitamin D in children. [ABSTRACT FROM AUTHOR]

Characterization of the genes expressed in adipose tissue (AT) is key to understanding the pathogenesis of obesity and to developing treatments for this condition. Our objective was to compare the gene expression in visceral AT (VAT) between obese and normal-weight prepubertal children. A total of fifteen obese and sixteen normal-weight children undergoing abdominal elective surgery were selected. RNA was extracted from VAT biopsies. Microarray experiments were independently performed for each sample (six obese and five normal-weight samples). Validation by quantitative PCR (qPCR) was performed on an additional 10 obese and 10 normal-weight VAT samples. Of 1276 differentially expressed genes (p < 0.05), 245 were more than two-fold higher in obese children than in normal-weight children. As validated by qPCR, expression was upregulated in genes involved in lipid and amino acid metabolism (CES1, NPRR3 and BHMT2), oxidative stress and extracellular matrix regulation (TNMD and NQO1), adipogenesis (CRYAB and AFF1) and inflammation (ANXA1); by contrast, only CALCRL gene expression was confirmed to be downregulated. In conclusion, this study in prepubertal children demonstrates the up- and down-regulation of genes that encode molecules that were previously proposed to influence the pathogenesis of adulthood obesity, as well as previously unreported dysregulated genes that may be candidate genes in the aetiology of obesity. [ABSTRACT FROM AUTHOR]

ObjectiveTo evaluate the association between waist-to-height ratio (WHtR) and specific biomarkers of inflammation, CVD risk and endothelial dysfunction in prepubertal obese children.DesignProspective, multicentre case–control study matched by age and sex.SettingChildren were recruited between May 2007 and May 2010 from primary-care centres and schools in three cities in Spain (Cordoba, Santiago de Compostela and Zaragoza).SubjectsFour hundred and forty-six (223 normal weight and 223 obese) Caucasian prepubertal children aged 6–12 years.ResultsWHtR was higher in the obese than in the normal-weight children. Blood pressure, waist circumference, weight, height, insulin, plasma lipids, leptin, resistin, abnormal neutrophil and monocyte counts, C-reactive protein, IL-6, IL-8, TNF-α, myeloperoxidase, soluble intercellular adhesion molecule-1, selectin and plasminogen activator inhibitor-1 levels were higher in the obese than in the normal-weight group. Adiponectin and HDL-cholesterol were lower and glucose and metalloproteinase-9 showed no differences. Resistin, TNF-α and active plasminogen activator inhibitor-1 were associated with WHtR, a sensitive indicator of central obesity.ConclusionsOur results lead to the hypothesis that changes in biomarker levels of insulin resistance, inflammation and CVD risk before puberty might induce metabolic consequences of obesity in obese children before reaching adulthood. [ABSTRACT FROM AUTHOR]

Background Variants in the FTO gene have been associated with obesity in children, but this association has not been shown with other biomarkers. We assessed the association of 52 FTO polymorphisms, spanning the whole gene, with obesity and estimated the influence of these polymorphisms on anthropometric, clinical and metabolic parameters as well as inflammation and cardiovascular disease (CVD) risk biomarkers among Spanish children. Methods A multicentre case-control study was conducted in 534 children (292 obese and 242 with normal-BMI). Anthropometric, clinical, metabolic, inflammation and CVD risk markers were compared using the Student's t-test for unpaired samples. The genotype relative risk was assessed by comparing the obese and normal-BMI group, calculating the odds ratio. The association of each SNP with phenotypic parameters was analysed using either logistic or linear regression analysis. Results All anthropometric, clinical and metabolic factors as well as inflammatory and CVD risk biomarkers were higher in the obese than in the normal-BMI group, except adiponectin and HDL-c that were lower, and glucose, LDL-c, and metalloproteinase-9 that did not show difference. Four polymorphisms (rs9935401, rs9939609, rs9928094 and rs9930333) were positively associated with obesity and in linkage disequilibrium between each other; the haplotype including the risk alleles of these polymorphisms showed a high risk for obesity. The rs8061518 was negatively associated with obesity and the haplotype including this SNP and rs3826169, rs17818902 and rs7190053 showed a decreased risk for obesity. Additionally, the rs8061518 was associated with weight, diastolic blood pressure, insulin, homeostatic model assessment of insulin resistance, leptin, and active plasminogen inhibitor activator-1 after sex and age adjustment; however, after an additional BMI adjustment, this polymorphism remained associated only with leptin. Conclusions We validated the previous reported association of genetic variability in intron 1 of the FTO gene with the risk of obesity and found no association with other related traits in this region of the gene. We have observed strong statistical evidence for an association of rs8061518 in intron 3 of the gene with decreased risk of obesity and low concentration of leptin. [ABSTRACT FROM AUTHOR]

Highlights: [•] We confirm the association of rs16147 with obesity in a cohort of Spanish children. [•] We demonstrate for the first time an association of rs16131 with childhood obesity. [•] rs16131 might have a possible impact on the early onset of obesity. [•] rs16131 might have a possible impact on the early onset of metabolic syndrome features. [Copyright &y& Elsevier]

This review focuses on metabolic differences of adipose tissue at different sites of the body, with emphasis in pediatrics. Adipose tissue is composed of various cell types, which include adipocytes and other cells of the stromal vascular fraction such as preadipocytes, blood cells, endothelial cells and macrophages. Mammals have two main types of adipose tissue: white adipose tissue (WAT), and brown adipose tissue (BAT), each of which possesses unique cell autonomous properties. WAT and BAT differ at the functional, as well as the morphological and molecular levels. WAT accumulates surplus energy mainly in the form of triacylglycerols and BAT dissipates energy directly as heat. Recently, functional BAT in humans has been located in the neck, supraclavicular, mediastinal and interscapular areas. WAT is distributed throughout the body in the form of two major types: subcutaneous adipose tissue (SWAT) and the intra-abdominal visceral adipose tissue (VWAT). VWAT tissue is associated with insulin resistance, diabetes mellitus, dyslipidaemia, hypertension, atherosclerosis, hepatic steatosis, and overall mortality whereas SWAT and BAT have intrinsic beneficial metabolic properties. Subcutaneous and visceral adipocytes derive from different progenitor cells that exhibit a different gene expression pattern. SWAT responds better to the antilipolytic effects of insulin and other hormones, secrets more adiponectin and less inflammatory cytokines, and is differentially affected by molecules involved in signal transduction as well as drugs compared with VWAT. Current research is investigating various approaches of BAT and SWAT transplantation, including new sources of adipocyte progenitors. This may be important for the potential treatment of childhood obesity. [ABSTRACT FROM AUTHOR]

Introduction: [ABSTRACT FROM AUTHOR]

Oxidative stress could help explain the relationship between childhood obesity and a metabolically unhealthy (MU) status. Moreover, puberty could also influence this relationship, since it entails physiological cardiometabolic changes. We aimed to evaluate plasma antioxidants and oxidative stress biomarkers in MU and metabolically healthy (MH) prepubertal and pubertal children and their associations with pro-inflammatory and endothelial damage biomarkers, taking puberty into account. A total of 1444 Spanish children aged 3–17 years (48.9% males, 66% prepubertal, 47.1% with obesity) were recruited. Blood pressure, anthropometric and biochemical parameters were measured, and children were categorized as having a MU or MH status according to risk factors. Retinol, carotenes, tocopherols, total antioxidant capacity (TAC), oxidized low-density lipoprotein and selected pro-inflammatory and endothelial damage biomarkers were analyzed. General linear models adjusted for age, sex, recruitment center and body mass index, partial correlations and stepwise linear regressions were performed. Lower carotenes and tocopherols levels were found in MU than in MH children. Plasma TAC was lower in prepubertal and higher in pubertal children with obesity compared to normal-weight children. Antioxidants and oxidative stress biomarkers showed novel associations with several pro-inflammatory and endothelial damage biomarkers, with pubertal differences, supporting the importance of considering both the antioxidant and oxidative stress status and puberty in the prevention of metabolic diseases in childhood. [ABSTRACT FROM AUTHOR]

Polygenetic risk scores (pGRSs) consisting of adult body mass index (BMI) genetic variants have been widely associated with obesity in children populations. The implication of such obesity pGRSs in the development of cardio-metabolic alterations during childhood as well as their utility for the clinical prediction of pubertal obesity outcomes has been barely investigated otherwise. In the present study, we evaluated the utility of an adult BMI predisposing pGRS for the prediction and pharmacological management of obesity in Spanish children, further investigating its implication in the appearance of cardio-metabolic alterations. For that purpose, we counted on genetics data from three well-characterized children populations (composed of 574, 96 and 124 individuals), following both cross-sectional and longitudinal designs, expanding childhood and puberty. As a result, we demonstrated that the pGRS is strongly associated with childhood BMI Z-Score (B = 1.56, SE = 0.27 and p-value = 1.90 × 10−8), and that could be used as a good predictor of obesity longitudinal trajectories during puberty. On the other hand, we showed that the pGRS is not associated with cardio-metabolic comorbidities in children and that certain environmental factors interact with the genetic predisposition to the disease. Finally, according to the results derived from a weight-reduction metformin intervention in children with obesity, we discarded the utility of the pGRS as a pharmacogenetics marker of metformin response. [ABSTRACT FROM AUTHOR]

S100A4 is a metastasis-associated protein also reported as a promising marker for dysfunctional white adipose tissue (WAT) and insulin resistance (IR) in adult and adolescent populations. We aimed to evaluate the association between the protein S100A4 and obesity and IR in children and during pubertal development. The study design consisted of three cross-sectional populations of 249, 11 and 19 prepubertal children respectively (named study population 1, 2 and 3), and a longitudinal population of 53 girls undergoing sexual maturation (study population 4). All subjects were classified into experimental groups according to their sex, obesity and IR status. All study populations counted on anthropometry, glucose, and lipid metabolism, inflammation and cardiovascular biomarkers as well as S100A4 plasma levels measured. The study population 1 was intended as the discovery population in which to elucidate the relationship between Obesity-IR and S100A4 plasma levels in prepubertal children. The cross-sectional populations 2 and 3 further counted on WAT gene expression data for investigating the molecular basis of this association. Instead, the longitudinal study population 4 presented blood whole-genome DNA methylation data at each temporal record, allowing deepening into the Obesity-IR-S1004 relationship during puberty as well as deciphering plausible epigenetic mechanisms altering S100A4 plasma levels. S100A4 plasma levels were strongly associated with several metabolic and anthropometric outcomes, namely IR, in prepubertal non-diabetic obese children. We also found highly significant positive associations during the course of puberty between the increase in S100A4 levels and the increase in HOMA-IR (P = 0.0003, FDR = 0.005) and insulin levels (P = 0.0003, FDR = 0.005). Methylation in two-enhancer related CpG sites of the S100A4 region (cg07245635 and cg10447638) was associated with IR biomarkers at the prepubertal stage and with longitudinal changes in these measurements. We further reported an association between visceral WAT (vWAT) S100A4 expression and HOMA-IR, insulin levels and BMI Z -Score, but not with circulating S100A4. We report for the first time the association of S100A4 with IR and WAT dysfunction in prepubertal populations as well as how the change in plasma S100A4 levels accompanies longitudinal trajectories of IR in children during pubertal development. Moreover, we propose epigenetic changes in two methylation sites and an altered S100A4 vWAT expression as plausible molecular mechanisms underlying this disturbance in obesity. • S100A4 is a protein associated with insulin resistance in children with obesity. • Change in plasma S100A4 levels accompanies longitudinal trajectories of IR in children during pubertal development. • Differential methylation of the S100A4 genetic region associates with IR in children with obesity. • Altered S100A4 vWAT expression also presents as a plausible molecular mechanism underlying IR in obesity. • S100A4 could serve as an early-life predictive marker for the appearance of IR and type-2-diabetes later in life. [ABSTRACT FROM AUTHOR]

X chromosome genetic variation has been proposed as a potential source of missing heritability for many complex diseases, including obesity. Currently, there is a lack of public available genetic datasets incorporating X chromosome genotype data. Although several X chromosome-specific statistics have been developed, there is also a lack of readily available implementations for routine analysis. Here, we aimed: (1) to make public and describe a dataset incorporating phenotype and X chromosome genotype data from a cohort of 915 normal-weight, overweight and obese children, and (2) to deeply describe a whole implementation of the special X chromosome analytic process in genetics. Datasets and pipelines like this are crucial to get familiar with the steps in which X chromosome requires special attention and may raise awareness of the importance of this genomic region. Design Type(s) disease analysis objective • factorial design • genetic structural variation analysis objective • genotyping design Measurement Type(s) genotyping assay Technology Type(s) genotyping Factor Type(s) sex • experimental condition Sample Characteristic(s) Homo sapiens • blood Machine-accessible metadata file describing the reported data (ISA-Tab format) [ABSTRACT FROM AUTHOR]

Introduction: the recent economic and financial crisis has affected most Western countries, especially families of low socioeconomic classes. We speculate that worsening of socioeconomic condition associated with the crisis would increase obesity, mainly in disadvantaged families.Material and Methods: cross-sectional study of the 290,111 children aged three to 12 years old attending public school during the term 2014-2015 in Madrid City, by means of a stratified weighted sample randomly chosen, taking into account age (grade), city district and schools. The questionnaire included weight and height (auto-reported), dietary report (weekly frequency of intake), as well as socioeconomic variables.Results: 1,208 questionnaires were evaluated from 64 classes. Half of participants were boys; 42% were younger than five years old, 35% werebetween six and eight years old, and 23% older than eight. Undernutrition was present in 5.0%, and excess of weight (overweight + obesity) in 36.7%. Undernutrition was higher in children under the age of six (9.1%). No relationship was found between undernutrition and the characteristics of the families but was slightly higher in families where both parents were unemployed. Excess of weight was higher in children of non-Spaniard parents (44% vs 32%, p < 0.0001), as well as in those families with economic problems (41% vs 31%, p = 0.0005). Only for meat, grains and dairy, the weekly intake was close to the recommendations.Conclusions: children from lower income households were at a higher risk of being overweight compared with their peers. Participation in a school-based food aid program may reduce food insecurity for children and their families. [ABSTRACT FROM AUTHOR]