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Adiponectin-cre FTO flox/flox and FTO flox/flox mouse white fat tissues

ABSTRACT: Single nucleotide polymorphisms in intron 1 of the fat mass and obesity-associated (FTO) gene were found to be associated with an increased risk of adult obesity. Enhanced FTO expression in mice leads to hyperphagia, increased fat mass, and higher body weight. Neuronal-specific FTO–deleted mice have an identical lean body weight phenotype to global FTO-deleted mice. The physiological role of adipose FTO in the homeostasis of energy regulation remains to be elucidated. We used microarrays to elucidate the metabolic pathways that are regulated by FTO in the white fat.

ORGANISM(S): Mus musculus

PROVIDER: GSE65098 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA272993

REPOSITORIES: GEO

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Adiponectin-cre FTO flox/flox and FTO flox/flox mouse white fat tissues

Project description:Single nucleotide polymorphisms in intron 1 of the fat mass and obesity-associated (FTO) gene were found to be associated with an increased risk of adult obesity. Enhanced FTO expression in mice leads to hyperphagia, increased fat mass, and higher body weight. Neuronal-specific FTOâ??deleted mice have an identical lean body weight phenotype to global FTO-deleted mice. The physiological role of adipose FTO in the homeostasis of energy regulation remains to be elucidated. We used microarrays to elucidate the metabolic pathways that are regulated by FTO in the white fat. FTO flox/flox and Adiponectin-cre FTO flox/flox (AFO) mice were fed with chow diet. White fat tissues from epididymal adipose pad were harvested under ad lib condition for RNA isolation. Three independent pools of FTO flox/flox and AFO mouse white fat RNA were included in the study.

2016-07-03 | E-GEOD-65098 | biostudies-arrayexpress

FTO regulates adult neurogenesis through modulating the dynamics of N6-methyladenosine

Project description:Fat mass and obesity-associated gene (FTO) is a member of the Fe (II) and oxoglutarate-dependent AlkB oxygenase family, and has been linked to obesity and intellectual disability. However, the role of FTO in neurodevelopment and neurogenesis remains largely unknown. Here, we show that FTO is expressed in adult neural stem cells (aNSCs) and neurons, and displays dynamic expression during postnatal neurodevelopment. The loss of FTO leads to the decreased brain size and body weight. We found that FTO deficiency could reduce the proliferation and neuronal differentiation of aNSCs in vivo, which leads to the impaired learning and memory. Given the role of FTO as a demethylase of N6-methyladenosine (m6A), we further performed the genome-wide m6A profiling and observed the dynamic m6A modification during postnatal neurodevelopment. The loss of FTO could lead to the altered m6A modifications on the mRNAs of several key components of BDNF pathway. These results together suggest that FTO play important roles in neurogenesis and learning and memory.

2017-04-20 | GSE94098 | GEO

Obesity-associated variants within FTO form long-range functional connections with IRX3

Project description:Genome-wide association studies in diverse populations have reproducibly associated variants within introns of FTO with increased risk for obesity and type-2 diabetes.While the molecular mechanisms linking these noncoding variants with obesity are not immediately obvious, subsequent studies in mice demonstrated that FTO expression levels influence body mass and composition phenotypes. Yet, no direct connection between the obesity-associated intronic variants and FTO expression or function has been made. We show that the obesity-associated noncoding sequences within FTO are functionally connected, at megabase distances, primarily with the homeobox gene IRX3, rather than with FTO. 4C-seq samples for Fto/fto and Irx3/irx3a genes promoters in different samples: adult mouse brain, E9.5 mouse embryos and 24hpf zebrafish embryos.

2014-02-24 | E-GEOD-52830 | biostudies-arrayexpress

FTO: gene expression and function in skeletal muscle

Project description:We identified the target genes of FTO ("fat mass and obesity associated") in primary cultures of human skeletal muscle cells using adenoviral vectors expressing FTO or GFP and oligonucleotide microarrays. Human myotubes were prepared from 4 different skeletal muscle biopsies. After differentiation, myotubes were infected for 48 hours with recombinant adenovirus expressing either GFP or FTO. Each FTO-infected myotubes culture was compared to GFP-infected myotubes culture. GFP-infected myotubes were regarded as the control. Four biological replicates were processed.

2011-07-05 | E-GEOD-22857 | biostudies-arrayexpress

FTO: gene expression and function in skeletal muscle

2011-07-05 | GSE22857 | GEO

Obesity-associated variants within FTO form long-range functional connections with IRX3

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FTO over expression in mice

Project description:In this study, we aimed to examine the changes in gene expression that occur in FTO over expressing mice in order to gain more insight into the underlying mechanisms by which FTO influences body weight and adiposity

2014-06-01 | E-MTAB-2331 | biostudies-arrayexpress

Role of FTO in ovarian cancer (MeRIP-Seq)

Project description:RNA methylation plays an important role fine tuning translation and subsequently regulating cellular responses and cell fate. The fat mass- and obesity-associated protein (FTO) was recognized as an m6A demethylase and described as an oncogenic factor in leukemia and brain tumors. FTO expression levels are suppressed in ovarian tumors and ovarian cancer stem cells (CSCs). FTO induce cyclic AMP activity through targeting PDE4B and PDE1C by down-regulation of m6A levels in the mRNA transcript. In all or findings point to a tumor suppressor function of FTO in high grade serous OC

2020-07-01 | GSE130349 | GEO

Role of FTO in ovarian cancer (RNA-Seq)

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An obesogenic FTO allele causes accelerated development, growth and insulin resistance in human skeletal muscle cells

Project description:Human GWAS have shown that obesogenic FTO polymorphisms correlate with lean mass, but the mechanisms have remained unclear. It is counterintuitive because lean mass is inversely correlated with obesity and metabolic diseases. Here, we use CRISPR to knock-in FTOrs9939609-A into hESC-derived tissue models, to elucidate potentially hidden roles of FTO during development. We find that among human tissues , FTOrs9939609-A most robustly affect human muscle progenitors’ proliferation, differentiation, senescence, thereby accelerating muscle developmental and metabolic aging. An edited FTOrs9939609-A allele over-stimulates insulin/IGF signaling via increased muscle-specific enhancer H3K27ac, FTO expression and m6A demethylation of H19 lncRNA and IGF2 mRNA, with excessive insulin/IGF signaling leading to insulin resistance upon replicative aging or exposure to high fat diet. This FTO-m6A-H19/IGF2 circuit may explain paradoxical GWAS findings linking FTOrs9939609-A to both leanness and obesity. Our results provide a proof-of-principle that CRISPR-hESC-tissue platforms can be harnessed to resolve puzzles in human metabolism.

2024-10-15 | GSE262261 | GEO

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