Expression data from childhood obesity
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ABSTRACT:
PROVIDER: PRJNA413927 | ENA |
REPOSITORIES: ENA
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Project description:In the past few decades, the prevalence of overweight and obesity has sharply increased in children and adolescents. Childhood obesity life are associated with increased risk of cardiovascular disease (CVD), diabetes mellitus, metabolic syndrome, sleep disturbances and certain cancers in adulthood. Childhood obesity has become a serious global public health challenge. Long noncoding RNAs (lncRNAs) have an important role in adipose tissue function and energy metabolism homeostasis, and abnormalities may lead to obesity. We used microarrays to detail the differential expression profile of lncRNAs and mRNAs in obese children compared with non-obese children.
2018-06-14 | GSE104815 | GEO
Project description:LEP-MCH conditioned childhood obesity
| PRJEB50693 | ENA
Project description:Childhood obesity is a major public health challenge, that increases the risk of comorbidities such as type 2 diabetes and cardiovascular disease, which collectively reduce life expectancy. Epigenetic mechanisms have been proposed as contributors to obesity-related long-term metabolic dysfunction. We performed DNA methylation profiling in whole blood from prepubertal children with obesity and normal weight controls, and identified 109 CpG sites associated with obesity. Two of these sites showed evidence of playing a causal role in mediating childhood obesity, as supported by two-sample Mendelian randomization test. Strikingly, both CpGs mapped within the same gene: Spermatogenesis and Centriole Associated 1 Like (SPATC1L). Further, we validated the causal CpGs in an independent clinical cohort. Together, these data suggest the SPATC1L locus might be a novel potential region playing a causal role on obesity development. To functionally confirm causality, we performed CRISPR/Cas9-mediated editing of these CpG sites. Their modification downregulated SPATC1L and neighbouring collagen genes (COL6A1, COL6A2), previously implicated in childhood obesity, and promoted higher lipid accumulation and insulin resistance in vitro. Following CpG editing, activating histone marks (H3K27Ac, H3K4me3) were reduced at the promoters of these genes, suggesting that these CpG sites regulate their expression through chromatin-mediated mechanisms. n summary, our study identifies the SPATC1L–COL locus as a novel causal region in childhood obesity and highlights mechanistic links between CpG methylation, histone modifications, deregulation of collagen gene expression, and metabolic dysfunction.
2026-05-04 | GSE329212 | GEO
Project description:Analysis of rectus femoris samples from chidren with obesity and normal weight. Obese children display insulin resistance (IR) and other metabolic abnormalities at higher rates than do normal weight children. Results provide insight into the molecular mechanisms underlying the pathogenesis of childhood obesity.
2022-01-31 | GSE139400 | GEO
Project description:Background: Childhood obesity is a critical public health issue that detrimentally affects muscle growth and function. Although the condition is widely prevalent, the specific mechanisms through which obesity induces these muscular impairments, as well as effective prevention strategies, remain insufficiently explored. Methods: We conducted a cross-sectional analysis of 155 children, categorized into obese and normal-weight groups, to evaluate the relationship between obesity and muscle health parameters. Concurrently, we established a murine model of obesity by exposing 3- and 8-week-old mice to a high-fat diet (HFD) to investigate the underlying mechanisms behind obesity’s effects on muscle mass, structure, and function. Additionally, vitamin C supplementation was explored as a potential preventative strategy against HFD-induced muscle impairments. Results: In juvenile mice, a HFD significantly increased both body and intramuscular fat while decreasing relative muscle mass and strength, mirroring the patterns observed in obese children. The diet downregulated key myogenic regulatory factors (MRFs) and myosin heavy chains (MHCs) in muscle tissue, alongside an upregulation of adipogenic pathways, contributing to impaired muscle growth and function. Notably, these adverse effects persisted into adulthood despite subsequent weight loss, underscoring the long-term impact of early dietary interventions. In contrast, adult mice did not exhibit significant muscular impairments after 4 weeks of HFD, suggesting age-specific dietary responses. Vitamin C supplementation effectively ameliorated these HFD-induced impairments in juvenile mice, enhancing muscle function and modifying gene expression related to muscle growth and fat metabolism. Conclusion: These results demonstrate that childhood obesity impairs muscle growth and function by altering myogenic and adipogenic pathways, effects which vitamin C supplementation can mitigate. Further research is needed to explore how a HFD induces these impairments, potentially through mechanisms such as fat accumulation and inflammation.
2026-04-22 | GSE280926 | GEO
Project description:The ch12q13 obesity locus is among the most significant childhood obesity loci identified in genome-wide association studies. This locus resides in a non-coding region within FAIM2; thus, the underlying causal variant(s) presumably influence disease susceptibility via an influence on cis-regulation within the genomic region. We implicated rs7132908 as a putative causal variant at this locus leveraging a combination of our inhouse 3D genomic data, public domain datasets, and several computational approaches. Using a luciferase reporter assay in human primary astrocytes, we observed allele-specific cis-regulatory activity of the immediate region harboring rs7132908. Motivated by this finding, we went on to generate isogenic human embryonic stem cell lines homozygous for either rs7132908 allele with CRISPR-Cas9 homology-directed repair to assess changes in gene expression due to genotype and chromatin accessibility throughout a differentiation to hypothalamic neurons, a key cell type known to regulate feeding behavior. We observed that the rs7132908 obesity risk allele influenced the expression of FAIM2 along with other genes, decreased the proportion of neurons produced during differentiation, up-regulated cell death gene sets, and conversely down-regulated neuron differentiation gene sets. We have therefore functionally validated rs7132908 as a causal obesity variant which temporally regulates nearby effector genes at the ch12q13 locus and influences neurodevelopment and survival.
2024-03-29 | GSE241593 | GEO
Project description:The ch12q13 obesity locus is among the most significant childhood obesity loci identified in genome-wide association studies. This locus resides in a non-coding region within FAIM2; thus, the underlying causal variant(s) presumably influence disease susceptibility via an influence on cis-regulation within the genomic region. We implicated rs7132908 as a putative causal variant at this locus leveraging a combination of our inhouse 3D genomic data, public domain datasets, and several computational approaches. Using a luciferase reporter assay in human primary astrocytes, we observed allele-specific cis-regulatory activity of the immediate region harboring rs7132908. Motivated by this finding, we went on to generate isogenic human embryonic stem cell lines homozygous for either rs7132908 allele with CRISPR-Cas9 homology-directed repair to assess changes in gene expression due to genotype and chromatin accessibility throughout a differentiation to hypothalamic neurons, a key cell type known to regulate feeding behavior. We observed that the rs7132908 obesity risk allele influenced the expression of FAIM2 along with other genes, decreased the proportion of neurons produced during differentiation, up-regulated cell death gene sets, and conversely down-regulated neuron differentiation gene sets. We have therefore functionally validated rs7132908 as a causal obesity variant which temporally regulates nearby effector genes at the ch12q13 locus and influences neurodevelopment and survival.
2024-03-29 | GSE241591 | GEO
Project description:Childhood Cancer Data Initiative (CCDI): PIVOT MSKCC
| PRJNA915175 | ENA
Project description:Childhood Cancer Data Initiative (CCDI): PIVOT MSKCC
| PRJNA915176 | ENA
Project description:SNP array data from 12 childhood adrenocortical tumors (ACT) were used to identify recurrent chromosome rearrangements and candidate driver genes.
2012-04-02 | GSE35064 | GEO