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The role of oxidative stress is well known in the pathogenesis of acquired malnutrition. Intrauterine growth restriction has been associated with an imbalance in oxidative stress/antioxidant system. Therefore, early postnatal environment and, consequently, extrauterine growth restriction might be associated with alterations in the antioxidant defense system, even in the prepubertal stage. This is a descriptive, analytical, and observational case–control study. The study included two groups; 38 Caucasian prepubertal children born prematurely and with a history of extrauterine growth restriction as the case group, and 123 gender- and age-matched controls. Plasma exogenous antioxidant (retinol, β-carotene, and α-tocopherol) concentrations were measured by HPLC; antioxidant enzyme activities of catalase, glutathione reductase, glutathione peroxidase, and superoxide dismutase were determined in lysed erythrocytes by spectrophotometric techniques. Catalase and glutathione peroxidase concentrations were significantly lower in extrauterine growth restriction children than in controls (P

The 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme catalyses the regeneration of active cortisol from inert cortisone and plays a critical role in tissue-specific corticosteroid reactions; therefore, 11β-HSD1 is a key molecule associated with the development of obesity. Despite evidence for its role in obesity, no genetic polymorphisms have been significantly associated with the disease per se.The aim of this study was to evaluate whether HSD11B1 gene variants, which have never been studied before, are associated with obesity and its related traits, as well as its relation to biomarkers of inflammation, liver damage and cardiovascular disease in a cohort of Spanish children.We performed a prospective case-control study.A total of 534 children were examined and classified as being obese (n=292) or normal weight (n=242). Anthropometric and biochemical measurements related to obesity, including inflammation, liver damage and cardiovascular disease, were determined. Genomic DNA was extracted and 10 HSD11B1 gene single-nucleotide polymorphisms (SNPs) were genotyped.A novel SNP, rs3753519, was strongly associated with obesity and this SNP was the only statistically significant HSD11B1 gene SNP remaining after a Bonferroni correction (odds ratio=1.97 for allelic effect, 95% confidence interval 1.23-3.16; P=0.004 and Bonferroni corrected P=0.046). In addition, this SNP was significantly and positively associated with increased body mass index (BMI), BMI z-score, weight, waist circumference, plasma γ-glutamyl transpeptidase and plasma active plasminogen activator inhibitor 1. The SNP was negatively associated with plasma adiponectin and cortisol after adjusting for sex and age. None of the inflammation biomarkers tested were associated with the risk allele.These data, which link an HSD11B1 genotype with both disease prevalence and its related phenotypes, strongly support a role for the rs3753519 polymorphism in the pathogenesis of pediatric-onset obesity.

Intense aerobic exercise has been found to prompt changes in oxidative stress, but in children remains almost unexplored. The aim was to investigate the effect of intense physical exercise on reduced glutathione (GSH as a biomarker of oxidative stress) and adrenocortical response (to verify a certain level of stress after exercise) in 38 prepubescent and 32 pubescent non-athlete boys. Four subgroups were established as puberty stage and physical fitness. Saliva samples were taken before and after incremental exercise testing to measure GSH, and cortisol levels. Saliva reduced glutathione levels were lower in all subgroups after exercise except in the prepubescent average fit group, significance being greater in the pubescent (P < 0.001) than in the prepubescent group (P < 0.01). Saliva cortisol increased after exercise in all except in the prepubescent “average fit” group. Physical exercise may give rise to oxidative stress and adrenocortical response in pubescent and prepubescent boys, depending on the duration and intensity of the test.

To evaluate the intake, plasma concentrations and postprandial response of trans fatty acids in obese and control children at prepubertal age in order to detect potential associations with childhood obesity.Case-control study, clinical dietary intervention with a 428 kcal standardized breakfast and longitudinal 3 h postprandial follow-up for trans fatty acid plasma levels.Fifty-four children aged 6-13 years of both sexes, 34 obese (body mass index97th percentile for age and sex) and 20 non-obese (control group) at prepubertal period (Tanner I).Various anthropometric parameters and sex hormones, fasting insulin and glucose, estimation of dietary trans fatty acid intake and their plasma quantitation in fasting conditions, and for 3 h following intake of a standardized breakfast.Dietary trans fatty acid intake was less than 0.4% of total energy in both groups, with a trend towards higher intake in obese children. Fasting plasma trans fatty acid concentrations and percentages were similar in both groups. However, trans fatty acid levels at +3 h were significantly higher than at 0 h in obese children, but not in controls (obese, 0 h: 2.38+/-0.29; 3 h: 3.62+/-0.45; controls, 0 h: 2.29+/-0.24; 3.14+/-0.49 mg/dl); cis monounsaturated fatty acid concentrations were not significantly affected by the postprandial interval. Obese children exhibited hyperinsulinemia and insulin resistance; however, trans fatty acid intake or their plasma levels were not associated with them.There is a low intake of trans fatty acids in Southern Spanish children, which is supported by their low concentrations in plasma. No difference in trans fatty acid intake is observed between obese and control children, although plasma levels remain higher in obese than in control children after 3 h of a meal. A marked insulin resistance is seen in obese, but it is not correlated with either trans fatty acid intake or plasma concentration.

OBJECTIVE: To review the mechanisms by which leptin, insulin and adiponectin influence lipid metabolism and plasma lipids in obesity, as well as to describe the associations between these hormones in prepubertal children. METHOD:Revision of relevant papers published in the last 5 y related to the interactions of leptin, insulin and adiponectin, with special emphasis on those reporting potential mechanisms by which these hormones regulate lipid metabolism and plasma lipids. We also provide original results concerning the relationships found between plasma lipids and leptin, and insulin and adiponectin in prepubertal obese children. RESULTS: Recent data in the literature shed new light to explain the effects of both leptin and adiponectin in the regulation of lipid metabolism in peripheral tissues. Activation of the AMP-dependent kinase pathway and subsequent increased fatty acid oxidation seems to be the main mechanism of action of these hormones in the regulation of lipid metabolism. In addition, we have found that insulin plasma levels are positively associated to leptin but negatively correlated with adiponectin in obese children. Adiponectin is negatively associated to plasma lipid markers of metabolic syndrome but positively related to HDL-cholesterol, whereas insulin and leptin show opposite patterns. These results support the effect of adiponectin in increasing insulin sensitivity and decreasing plasma triglycerides. CONCLUSION: Leptin, insulin and adiponectin are associated hormones that regulate lipid metabolism in childhood. Adiponectin appears to be the missing link to explain the alterations in lipid metabolism and plasma lipids seen in obesity.

Sirs, We have read with great interest the brief report of Boussemart et al. [1] published online first and strongly agree with their recommendation of strict vigilance of the fluid status in young patients with nephrogenic diabetes insipidus (NDI) who begin treatment. In fact, we would also recommend that not only are water balance and frequent clinical assessment, including hemodynamical status when necessary, crucial, but blood and urine sodium determination as well. The authors attribute their patient’s water intoxication to a strong enhanced sodium reabsorption due to the additive effect of hydrochlorothiazide and indomethacin combination therapy together with the lack of any physiological control of water intake secondary to gastric feeding. However, we experienced a water intoxication case in a 2-month-old male infant who only received initial hydrochlorothiazide treatment and was only bottle fed. Our patient was admitted to the hospital for evaluation of prolonged fever. Hypernatremia (Na 158 mEq/l) was revealed on admission, and a repeated medical history from their parents revealed that the infant had experienced polyuria–polydipsia since the first days of life, with a daily oral water intake of 500 ml added to his formula bottles, which they had considered normal. A dehydration test with subsequent 1-desamino-8-D-arginine vasopressin administration confirmed the diagnosis of NDI, and sequence analyses revealed mutation p.Trp200GlyfsX12 in exon 4 of the AVPR2 gene. Hydrochlorothiazide treatment was initiated at 2 mg/kg per day orally twice a day. Six hours after the first dose had been administered, the infant developed transient profuse sweating, paleness and hypothermia. The serum sodium concentration was 141 mEq/l at that time (pretreatment control 153 mEq/l), indicating water intoxication. Consequently, further hydrochlorothiazide treatment was stopped. The infant clinically recovered in the following hours. The treatment was reinitiated the following day at a lower dose, 1 mg/kg per day orally twice a day, which was well tolerated; no serum sodium control was obtained. The third day of treatment, 5 h after receiving the morning dose of hydrochlorothiazide, the patient's clinical condition worsened once again, with sweating, paleness, hypothermia, weakness, lethargy and gasping breathing. The serum sodium level was checked and the patient admitted to the pediatric intensive care unit (PICU). As the serum sodium concentration was 137 mEq/l, we were unable to demonstrate hyponatremia, but we hypothesized that there had probably been a significant serum sodium and subsequent osmolar shift secondary to water intoxication that had led to cerebral swelling. A cranial computerized scan showed no findings at that moment, and the patient recovered spontaneously during the following hours. Polyuria–polydipsia and hypernatremia continued the following days after the withdrawal of treatment. Therefore, 2 days later treatment was once again reinitiated at a lower dose (0.5 mg/kg per day twice a day). This treatment was well tolerated and was progressively increased during the following days (maximum 4 mg/kg per day) until neutral water balances were be achieved. Central venous catheter Pediatr Nephrol (2009) 24:2277–2278 DOI 10.1007/s00467-009-1236-4