Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DIDO is necessary for adipogenesis promoting diet-induced obesity [I]

ABSTRACT: Rates of overweight and obesity continue to rise in the population worldwide. Obesity reduces life expectancy because it is an important predisposing factor for cancer, cardiovascular diseases and diabetes mellitus. Adipose tissue (AT), the main organ for fat storage with endocrine capacity, plays fundamental roles in systemic metabolism and in obesity-related diseases. Adiposity and lipodystrophy are associated with metabolic disorders, indicating that normal AT function is required for metabolic health. Dido1 is a marker gene for stemness and gene-targeting experiments compromised several functions from cell division to embryonic stem cell differentiation, in vivo and in vitro. Using animals carrying a DIDO mutant without the N-terminal, we report that these mice display a lean phenotype with reduced adipose tissue and hypolipidemia even when fed with an obesogenic diet. The phenotype related to impaired adipogenesis, partially corrected by transcription factors C/EBPα or PPARγ expression and to hypothermia subsequent to dermal fat thinning. Deep sequencing of the epididymal white fat (Epi WAT) transcriptome shows the role of Dido1 in the control of cellular lipases. The molecular analysis involves Dido1 in orchestrating adipogenesis and altogether offers a model different from described lipodystrophies in mice and pioneers a new path to understand obesity and identify mechanism for obesity intervention.

ORGANISM(S): Mus musculus

PROVIDER: GSE195908 | GEO | 2024/01/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

DIDO is necessary for the adipogenesis that promotes diet-induced obesity

Project description:The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue (AT), the main fat storage organ with endocrine capacity, plays fundamental roles in systemic metabolism and obesity-related diseases. Dysfunctional AT can induce excess or reduced body fat (lipodystrophy). Dido1 is a marker gene for stemness; gene-targeting experiments compromised several functions ranging from cell division to embryonic stem cell differentiation, both in vivo and in vitro. We report that mutant mice lacking the DIDO N terminus show a lean phenotype. This consists of reduced AT and hypolipidemia, even when mice are fed a high-nutrient diet. DIDO mutation caused hypothermia due to lipoatrophy of white adipose tissue (WAT) and dermal fat thinning. Deep sequencing of the epididymal white fat (Epi WAT) transcriptome supported Dido1 control of the cellular lipid metabolic process. We found that, by controlling the expression of transcription factors such as C/EBPα or PPARγ, Dido1 is necessary for adipocyte differentiation, and that restoring their expression reestablished adipogenesis capacity in Dido1 mutants. Our model differs from other lipodystrophic mice and could constitute a new system for the development of therapeutic intervention in obesity.

2024-01-09 | GSE236036 | GEO

DIDO is necessary for the adipogenesis that promotes diet-induced obesity [II]

Project description:The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue (AT), the main fat storage organ with endocrine capacity, plays fundamental roles in systemic metabolism and obesity-related diseases. Dysfunctional AT can induce excess or reduced body fat (lipodystrophy). Dido1 is a marker gene for stemness; gene-targeting experiments compromised several functions ranging from cell division to embryonic stem cell differentiation, both in vivo and in vitro. We report that mutant mice lacking the DIDO N terminus show a lean phenotype. This consists of reduced AT and hypolipidemia, even when mice are fed a high nutrient diet. DIDO mutation caused hypothermia due to lipoatrophy of white adipose tissue (WAT) and dermal fat thinning. Deep sequencing of the epididymal white fat (Epi WAT) transcriptome supported Dido1 control of the lipid metabolic process. We found that, by controlling expression of transcription factors such as C/EBPα or PPARγ, Dido1 is necessary for adipocyte differentiation, and that restoring their expression reestablished adipogenesis capacity in Dido1 mutants. Our model differs from other lipodystrophic mice and could constitute a new system for the development of therapeutic intervention in obesity.

2024-01-09 | GSE236034 | GEO

DIDO is necessary for adipogenesis promoting diet-induced obesity [I]

Project description:DIDO is necessary for adipogenesis promoting diet-induced obesity [I]

| PRJNA802653 | ENA

DIDO is necessary for the adipogenesis that promotes diet-induced obesity

Project description:DIDO is necessary for the adipogenesis that promotes diet-induced obesity

| PRJNA988474 | ENA

DIDO is necessary for the adipogenesis that promotes diet-induced obesity [II]

Project description:DIDO is necessary for the adipogenesis that promotes diet-induced obesity [II]

| PRJNA988477 | ENA

Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (ChIP-seq)

Project description:Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation.

2017-03-16 | GSE85028 | GEO

Philaethria dido

Project description:Philaethria dido Genome sequencing and assembly

| PRJNA686711 | ENA

Loss of adipocyte-specific Olfactomedin-2 in obesity drives defective fat cell function, aggravating adipose tissue accretion

Project description:Olfactomedin-2 (OLFM2) participates in brain development and appears to be involved in energy handling. In adipose tissue, we here show expression of OLFM2 to be adipocyte-specific and opposed to obesity. OLFM2 levels are increased during adipogenesis, and impaired when differentiated fat cells are challenged with conditions emulating inflammation in the context of obesity. On the molecular level, examination of OLFM2 deficiency in human adipocytes indicated down-regulation of genes related to cell cycle. At the cellular level, the loss of OLFM2 compromised adipogenesis, while its over-production enhanced the adipogenic transformation of 3T3-L1 cells. Complementary loss and gain of function assays coupled to untargeted proteomics revealed the modulation of key protein pathways, including regulation of citrate cycle, fatty acid degradation, axon guidance and focal adhesion in mature adipocytes and precursor cells. Transferring these findings into animal models using a whole-body knockout and transcriptionally depleted adipose Olfm2 highlighted, respectively, a cluster of molecular changes connected with defective cell cycle (in both), fat mass accretion and impaired metabolism (in the latter). Our data underscores a key role for OLFM2 in fat cells, and suggests that the association between adipose OLFM2 and obesity is not only correlative but also causative.

2023-11-16 | MSV000093409 | MassIVE

Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (vsmutCT)

2017-03-16 | GSE85026 | GEO

Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (vsmut)

2017-03-16 | GSE85025 | GEO