LEP-MCH conditioned childhood obesity
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ABSTRACT:
PROVIDER: PRJEB50693 | 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:Expression data from childhood obesity
| PRJNA413927 | 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:In order to understand heterogeneity of MCH neurons, by using MCH-Cre dependent ZsGreen (fl/fl) reporter mice, we isolated nuclear from 16 hypothalami of 16 mice at the age of 16-18weeks. Through flow cytometry, we were able to distinguish ZsGreen positive nuclei, and collected puried MCH nuclei in suspension. Those nuclei suspension were subjected to single cell sequence by 10x™ GemCode™ Technology for further single nuleus mRNA analysis and unravel subclusters of MCH neurons
2020-05-07 | GSE146020 | GEO
Project description:Neuroendocrine regulation is essential for maintaining metabolic homeostasis. However, whether neuroendocrine pathway influence bone metabolism is unelucidated. Here, we identify a central neuroendocrine circuit that directly controls osteogenesis. Using virus based tracing, weidentify that melanin concentrating hormone (MCH) expressing neuronsin the lateral hypothalamus (LH) are connected to the bone.Chemogenetic activation of MCH neurons in the LH induces osteogenesis, whereas inhibiting these neurons reduces osteogenesis.Meanwhile, MCH is released into the circulation upon chemogenetic activation of these neurons. Single cell sequencing reveals that blocking MCH neurons in the LH diminishes osteogenic differentiation of bone marrow stromal cells (BMSCs). Mechanistically, MCH promotes BMSC differentiation by activating MCHR1 via PKA signaling and activating MCHR1 by MCH agonists attenuate osteoporosis in mice. By elucidating a brain-bone connection that autonomously enhances osteogenesis, these findings uncover the neuroendocrinological mechanisms governing bone mass regulation.
2025-08-01 | GSE239973 | GEO
Project description:We report phosphoRiboTrap experiments result which aim to explore the nature of the cell types in the Median Eminence (ME) regulated as a consequene of chemogenetic MCH neuron activation. Control and MCH-hM3Dq mice were 12 hrs-fasted and i.p. injected with CNO (3 mg/kg), Arcuate (ARC) and median eminence expat were extracted for preciptation of S6-marked ribosomes from both groups of mice. Extracted RNA from Immunoprecipitated ribosomes (IP) and total tissue (ARC+ME) from each mouse were subjected to deep mRNA sequencing. By analyzing the overlap of genes enriched in the IP/Input of MCH neuron activated mice with previously identified cell types using single cell mRNA sequencing of cells in the mediobasal hypothalamus (Campbell et al., 2017), we identified gene clusters which were activated upon MCH neuron activation.
2020-05-07 | GSE146019 | GEO
Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms. MeCP2 ChIP-Seq were conducted from ~ 7-week-old hypothalamus tissues from Mecp2-/y; MECP2-EGFP mice.
2015-04-15 | E-GEOD-66868 | biostudies-arrayexpress
Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms. Mnase-Seq were conducted from 7-week-old hypothalamus from MeCP2 knockout mice and their age and genetic background matched wild types control mice.
2015-04-15 | E-GEOD-66869 | biostudies-arrayexpress
Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms.
2015-04-15 | GSE66869 | GEO