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Adipose tissue-derived microRNAs as epigenetic modulators of type 2 diabetes

ABSTRACT: Diabetes-resistant and diabetes-prone female New Zealand Obese mice were assessed based on liver fat content and early blood glucose concentrations at 10 weeks of age before the onset of T2D. Analysis of the DNA methylation profile in gonadal white adipose tissue revealed that the imprinted region Dlk1-Gtl2 and Mest (miR-335) potentially regulated by DNA methylation.

ORGANISM(S): Mus musculus

PROVIDER: GSE310390 | GEO | 2025/12/17

REPOSITORIES: GEO

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Adipose tissue-derived microRNAs as epigenetic modulators of type 2 diabetes

Project description:White adipose tissue (WAT) dysfunction along with an aberrant expression of miRNAs are strongly associated with the risk of developing type 2 diabetes (T2D) with limited evidence linking early changes in the WAT-derived miRNAs and T2D. The present study aims to identify early miRNome changes prognostic for T2D in mice and humans. Gonadal (g) WAT of diabetes-resistant and -prone mice were subjected to multi-omics analyses (transcriptome, miRNome, methylome, proteome). Metabolic phenotypes linked with T2D were correlated with adipose tissue miRNA expression and DNA methylation from 14 monozygotic twin pairs discordant for T2D. Plasma miRNA levels from females at high risk of developing T2D (TÜF study) were included. Adipose tissue of the diabetes-susceptible mice was less insulin sensitive with 150 differentially expressed miRNAs compared to diabetes-resistant mice. Integrative analysis of miRNome-transcriptome-proteome identified 61 proteins involved in actin cytoskeleton, amino acid and sphingolipid metabolism. More than 20 miRNAs are located in the imprinted region Dlk1-Gtl2 and miR-335 in Mest and regulated by DNA methylation. Imprinted miRNAs also exhibited similar alteration in monozygotic twin pairs discordant for T2D with miR-335 expression altered only in females. Moreover, plasma levels of miR-335-5p were negatively correlated with fasting blood glucose in female individuals at high risk of developing T2D. Early alterations of WAT-derived miRNAs such as miR-335-5p could contribute to systemic metabolic changes associated with the risk of developing T2D.

2025-12-15 | PXD057291 | Pride

Adipose tissue-derived microRNAs as epigenetic modulators of type 2 diabetes [DPDR_smallSeq]

2025-12-17 | GSE310457 | GEO

Adipose tissue-derived microRNAs as epigenetic modulators of type 2 diabetes [3T3_RNASeq]

Project description:Diabetes-resistant and diabetes-prone female New Zealand Obese mice were assessed based on liver fat content and early blood glucose concentrations at 10 weeks of age before the onset of T2D. Analysis of the microRNA profile in gonadal white adipose tissue revealed miRNA-335-5p, which could contribute to systemic metabolic changes associated with the risk of developing T2D. Treatment of miR-335-5p mimic in 3T3-L1 cells led to elevated triglyceride accumulation on day 3 of adipogenesis. To elucidate the molecular mechanisms underlying the increased triglyceride accumulation, RNA sequencing was conducted at days 3 and 6 of cell differentiation. This analysis showed alterations in genes involved in lipid metabolism, glycolytic enzymes and ECM remodeling.

2025-12-17 | GSE310455 | GEO

Adipose tissue-derived microRNAs as epigenetic modulators of type 2 diabetes [DPDR_RNASEQ]

Project description:Diabetes-resistant and diabetes-prone female New Zealand Obese mice were assessed based on liver fat content and early blood glucose concentrations at 10 weeks of age before the onset of T2D. Transcriptome analysis of gonadal white adipose tissue revealed genes potentially regulated by epigenetic mechanisms such as miRNAs or DNA methylation.

2025-12-17 | GSE310456 | GEO

Epigenetic changes in Langerhans islets preceding the onset of diabetes

Project description:Diabetes-resistant and diabetes-prone female New Zealand Obese mice were classified based on liver fat content and early blood glucose concentrations at 10 weeks of age before the onset of T2D. By using transcriptome and DNA methylome analysis of Langerhans islets, we identified early epigenetic alteration in mice and humans which could serve as putative epigenetic biomarkers

2020-10-28 | GSE143875 | GEO

Differences in DNA methylation of HAMP in blood cells predicts the development of type 2 diabetes [WGBS]

Project description:Diabetes-resistant and diabetes-prone female New Zealand Obese mice were classified based on liver fat content and early blood glucose concentrations at 10 weeks of age before the onset of T2D. By using transcriptome and DNA methylome analysis of liver samples, we identified early epigenetic alteration in mice and humans which could serve as putative epigenetic biomarkers

2023-07-17 | GSE208628 | GEO

Differences in DNA methylation of HAMP in blood cells predicts the development of type 2 diabetes [RNA-seq]

Project description:Diabetes-resistant and diabetes-prone female New Zealand Obese mice were classified based on liver fat content and early blood glucose concentrations at 10 weeks of age before the onset of T2D. By using transcriptome and DNA methylome analysis of liver samples, we identified early epigenetic alteration in mice and humans which could serve as putative epigenetic biomarkers

2023-07-17 | GSE208627 | GEO

Paternally induced transgenerational inheritance of susceptibility to diabetes in mammals (MeDIP-Seq)

Project description:The global prevalence of type 2 diabetes (T2D) is increasing, and it is contributing to the susceptibility to diabetes and its related epidemic in offspring. Although the impacts of paternal T2D on metabolism of offspring have been well established, the exact molecular and mechanistic basis that mediates these impacts remains largely unclear. Here we show that paternal T2D increases the susceptibility to diabetes in offspring through the gametic epigenetic alterations. Paternal T2D led to glucose intolerance and insulin resistance in offspring. Relative to controls, offspring of T2D fathers exhibited altered gene expression patterns in the pancreatic islets, with downregulation of several genes involved in glucose metabolism and insulin signaling pathway. Epigenomic profiling of offspring pancreatic islets revealed numerous changes in cytosine methylation depending on paternal T2D, including reproducible changes in methylation over several insulin signaling genes. Paternal T2D altered overall methylome patterns in sperm, with a large portion of differentially methylated genes overlapped with that of pancreatic islets in offspring. Our study revealed, for the first time, that T2D can be inherited transgenerationally through the mammalian germline by an epigenetic manner. Examination of the effect of paternal T2D on the DNA methylation in the pancreatic islets of offspring and in the sperm of father.

2013-01-02 | E-GEOD-43238 | biostudies-arrayexpress

Assessing the effect of the CLPG mutation on the microRNA catalogue of skeletal muscle using high-throughput sequencing

Project description:The callipyge phenotype is a monogenic muscular hypertrophy that is only expressed in heterozygous sheep receiving the CLPG mutation from their sire. The wild-type phenotype of CLPG/CLPG animals is thought to result from translational inhibition of paternally expressed DLK1 transcripts by maternally expressed miRNAs. To identify the miRNA responsible for this trans-effect, we used high-throughput sequencing to exhaustively catalogue miRNAs expressed in skeletal muscle of sheep of the four CLPG genotypes. We have identified 747 miRNA species of which 110 map to the DLK1-GTL2 or callipyge domain. We demonstrate that the latter are imprinted and preferentially expressed from the maternal allele. We show that the CLPG mutation affects their level of expression in cis (~3.2-fold increase) as well as in trans (~1.8-fold increase). In CLPG/CLPG animals, miRNAs from the DLK1-GTL2 domain account for ~20% of miRNAs in skeletal muscle.We show that the CLPG genotype affects the levels of A to I editing of at least five pri-miRNAs of the DLK1-GTL2 domain, but that levels of editing of mature miRNA are always minor. We present suggestive evidence that the miRNAs from the domain target the ORF of DLK1 thereby causing the trans-inhibition underlying polar overdominance. We highlight the limitations of high-throughput sequencing for digital gene expression profiling as a result of biased and inconsistent amplification of specific miRNAs.

2010-09-24 | GSE24146 | GEO

A bipartite element with allele-specific functions safeguards DNA methylation imprints at the Dlk1-Dio3 locus [4C-seq]

Project description:Dysregulation of imprinted gene loci also referred to as loss of imprinting (LOI) can result in severe developmental defects and other diseases, but the molecular mechanisms that ensure imprint stability remain incompletely understood. Here, we dissect the functional components of the imprinting control region of the essential Dlk1-Dio3 locus (called IG-DMR) and the mechanism by which they ensure imprinting maintenance. Using pluripotent stem cells carrying an allele-specific reporter system, we demonstrate that the IG-DMR consists of two antagonistic regulatory elements: a paternally methylated CpG-island that prevents the activity of Tet dioxygenases and a maternally unmethylated regulatory element, which serves as a non-canonical enhancer and maintains expression of the maternal Gtl2 lncRNA by precluding de novo DNA methyltransferase function. Targeted genetic or epigenetic editing of these elements leads to LOI with either bi-paternal or bi-maternal expression patterns and respective allelic changes in DNA methylation and 3D chromatin topology of the entire Dlk1-Dio3 locus. Although the targeted repression of either IG-DMR or Gtl2 promoter is sufficient to cause LOI, the stability of LOI phenotype depends on the IG-DMR status, suggesting a functional hierarchy. These findings establish the IG-DMR as a novel type of bipartite control element and provide mechanistic insights into the control of Dlk1-Dio3 imprinting by allele-specific restriction of the active DNA (de)methylation machinery.

2021-09-14 | GSE148315 | GEO

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