Conclusions The significant associations between TSH, adiponectin and blood pressure, observed in children and adolescents from a population-based cohort, are attenuated or absent in children and adolescents with overweight or obesity, suggesting that childhood obesity distorts the healthy interplay between the thyroid axis, thyroid-adipokine interaction and blood pressure.
This study investigated whether the combined effects of FTO and MC4R increase the risk of obesity in children and adolescents living in Northwest China.
This meta-analysis aimed to examine and synthesize evidence on the association between these two common MC3R polymorphisms and the development of childhood obesity.
We aimed to investigate a possible sleep-gene interaction for childhood obesity risk, and whether the interaction in childhood longitudinally contributes to obesity risk at a 10-year follow-up and further to test if there is any mediation through the leptin pathway.
Four significant risk factors for OSA were identified: maternal obesity/diabetes during pregnancy (OR, 1.63; 95% CI, 1.21-2.21; P = .001), preterm/low birth weight (OR, 1.74; 95% CI, 1.30-2.32; P < .001), early childhood obesity (OR, 1.89; 95% CI, 1.37-2.62; P < .001), and high leptin levels in early childhood (OR, 1.94; 95% CI, 1.22-3.09; P = .005).
Meta-analysis of 2969 individuals with obesity and 2572 with normal weight showed a positive association between rare heterozygous coding partial/complete LOF mutations in MC3R and obesity in children and adults of European, North African, and Asian ancestries (odds ratio = 3.07; 95% CI, 1.48-7.00; P = 4.2 × 10<sup>-3</sup> ).
Mutations in melanocortin receptor (MC4R) are the most common cause of monogenic obesity in children of European ancestry, but little is known about their prevalence in children from the minority populations in the United States.
MC3R and MC4R are involved in metabolic regulation and their gene variants are associated with severe pediatric obesity, whereas the function of MC5R remains to be fully elucidated.
In conclusion, these results suggest that serum adiponectin levels modify the association between childhood obesity and adult atherosclerosis, which has implications for risk stratification and targeted intervention for obese children with low levels of adiponectin.
The present study evaluates the relationship between leptinG2548A (rs7799039) and leptin receptors (rs1137101" genes_norm="3953">Gln223Arg (rs1137101) genotyping and its leptin level and the risk of childhood obesity.
Mutations in the genes encoding leptin (LEP), the leptin receptor (LEPR), and the melanocortin 4 receptor (MC4R) are known to cause severe early-onset childhood obesity.
MC3R and MC4R are involved in metabolic regulation and their gene variants are associated with severe pediatric obesity, whereas the function of MC5R remains to be fully elucidated.
Mutations in the genes encoding leptin (LEP), the leptin receptor (LEPR), and the melanocortin 4 receptor (MC4R) are known to cause severe early-onset childhood obesity.
We showed that MC4Rrs17782313 and FTO rs9939609 were positively associated with zBMI, with weak and very weak effects, respectively, suggesting a very scarce contribution to childhood obesity.
From a previous proteomic study identifying adiponectin as a link between VDD and pediatric obesity, herein we analysed another protein (SSP2301) increased with VDD.
To the best of our knowledge, this is the first study investigating the relationship between circulating zonulin level (as a marker of intestinal permeability) and insulin resistance and leptin (as markers of metabolic disturbances associated with obesity) in childhood obesity.
The analysis was restricted to studies that examined the effect of exercise interventions on adipokines (adiponectin, leptin, resistin and visfatin) in pediatric obesity (6-18 years old).
We measured bioactive and immunoreactive leptin levels by enzyme-linked immunosorbent assays in fasting serum samples of 70 children with severe (BMI SDS >3) non-syndromic obesity with onset <3 years of life from our Leipzig childhood obesity cohort (n = 1204).
The combined presence of three or more high-risk alleles of both the FTO and MC4R genes confers a 4-fold higher risk for obesity in children and adolescents of Greek origin, although these risk alleles have no impact on the metabolic alterations observed in these obese children and adolescents.
We observed high population differentiation between European and African populations at two MC3Rchildhood obesity- and insulin resistance-associated single-nucleotide polymorphisms (rs3746619 and rs3827103) using Wright's F statistics.
Three known adult BMI-associated loci (FTO, MC4R and ADCY3) and one childhood obesity locus (OLFM4) reached genome-wide significance (PWald < 1.13 × 10(-8)) with BMI at 8 years and/or change over time.