Impact of dioxin exposure and high fat diet feeding on adult mouse islets
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA604802 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11018000.fastq.gz | Fastqsanger.gz | |||
| SRR11018001.fastq.gz | Fastqsanger.gz | |||
| SRR11018002.fastq.gz | Fastqsanger.gz | |||
| SRR11018003.fastq.gz | Fastqsanger.gz | |||
| SRR11018004.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: to determine whether chronic low dose dioxin exposure in adult male and female mice impacts susceptibility to metabolic disease and islet dysfunction.
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2018-10-02 | E-MTAB-6719 | biostudies-arrayexpress
Project description:The adipose tissue plays an important role in controlling whole-body energy balance, and proper regulation of adipose tissue function is essential for metabolic health. In response to energy surplus, the adipose tissue needs to expand, which may lead to local areas of hypoxia within the tissue. This is thought to promote whole-body insulin resistance. Here we report that DICER, a key enzyme in the maturation of miRNAs and a potential marker of adipocyte health, is profoundly downregulated in mouse adipose tissue within the first week of high-fat diet (HFD) feeding, and this effect is sustained in response to long-term HFD feeding. The downregulation of DICER protein occurs in both mature adipocytes and in the stromal vascular cells. Mechanistically, we provide evidence that hypoxia and hypoxia-inducible factor 1-α (HIF1α) facilitate ubiquitination of DICER to target it for autophagy-mediated degradation, and we show that DICER and HIF1α interact in adipose tissue after HFD feeding, which may signal for DICER degradation. Finally, despite reductions in DICER protein, we were not able to detect any differences in global miRNA levels in subcutaneous adipose tissue of mice after one or three weeks of HFD-feeding. In conclusion, the nutritional challenge of HFD feeding in mice leads to a large reduction in adipose tissue DICER protein, which is induced by hypoxia during tissue expansion and mediated through an interaction with HIF1α.
2024-11-12 | GSE254511 | GEO
Project description:Dioxin-like chemicals are well-known for their ability to upregulate expression of numerous genes via the AH receptor (AHR). However, recent transcriptomic analyses in several laboratories indicate that dioxin-like chemicals or AHR genotype itself also can downregulate levels of mRNAs encoded by numerous genes. The mechanism responsible for such downregulation is unknown. We hypothesized that microRNAs (miRNAs), which have emerged as powerful negative regulators of mRNA levels in several systems, might be responsible for mRNA downregulation in dioxin/AHR pathways. We used the Ambion miRNA array platform as well as quantitative RT-PCR to measure miRNA levels in dioxin-sensitive Long-Evans (Turku/AB; L-E) rats vs. dioxin-resistant Han/Wistar(Kuopio; H/W) rats. Treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in vivo caused no significant changes in miRNA levels in rat livers. AHR genotype had no effect on hepatic miRNA levels in response to TCDD – no miRNAs differed in expression between between L-E rats (that have wildtype AHR) compared to H/W rats (whose AHR has a large deletion in the transactivation domain). It is unlikely that mRNA downregulation by dioxins is mediated by miRNAs, nor are miRNAs likely to play a significant role in dioxin toxicity in adult rodent liver. Manuscript Submitted: Moffat ID, Boutros PC, Celius T, Pohjanvirta R & Okey AB. Micro-RNAs in rodent liver are refractory to dioxin treatment. Toxicological Sciences May, 2007. Keywords: miRNA expression, response to xenobiotics, genetic modification, comparative genome hybridization
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Project description:Dioxin is one of the most common historic industrial contaminants with several major industry and government accidents having exposed large numbers of the worldwide population over the past century. Previous rat studies have demonstrated the ability of dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)) exposure to promote the epigenetic transgenerational inheritance of disease susceptibility in subsequent generations. The types of disease observed include testis, ovary, kidney, prostate and obesity pathologies. The current study was designed to use an epigenome-wide association study (EWAS) to identify potential sperm DNA methylation biomarkers for specific transgenerational diseases. The transgenerational F3 generation dioxin lineage male rats with and without a specific disease were compared to identify differential DNA methylation regions (DMRs). The genomic features of the DMRs are characterized. Observations demonstrate that disease specific epimutation DMRs exist for the transgenerational dioxin lineage rats that can potentially be used as epigenetic biomarkers for testis, ovary, kidney, prostate and obesity diseases. These disease specific DMRs were associated with genes that have previously been shown to be linked with these diseases. This EWAS for transgenerational disease identified epigenetic biomarkers and provides the proof of concept of the potential to develop similar biomarkers for humans to diagnose disease susceptibilities and facilitate preventative medicine.
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Project description:Dioxin-like chemicals are well-known for their ability to upregulate expression of numerous genes via the AH receptor (AHR). However, recent transcriptomic analyses in several laboratories indicate that dioxin-like chemicals or AHR genotype itself also can downregulate levels of mRNAs encoded by numerous genes. The mechanism responsible for such downregulation is unknown. We hypothesized that microRNAs (miRNAs), which have emerged as powerful negative regulators of mRNA levels in several systems, might be responsible for mRNA downregulation in dioxin/AHR pathways. We used the Ambion miRNA array platform as well as quantitative RT-PCR to measure miRNA levels in dioxin-sensitive Long-Evans (Turku/AB; L-E) rats vs. dioxin-resistant Han/Wistar(Kuopio; H/W) rats. Treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in vivo caused no significant changes in miRNA levels in rat livers. AHR genotype had no effect on hepatic miRNA levels in response to TCDD – no miRNAs differed in expression between between L-E rats (that have wildtype AHR) compared to H/W rats (whose AHR has a large deletion in the transactivation domain). It is unlikely that mRNA downregulation by dioxins is mediated by miRNAs, nor are miRNAs likely to play a significant role in dioxin toxicity in adult rodent liver. Manuscript Submitted: Moffat ID, Boutros PC, Celius T, Pohjanvirta R & Okey AB. Micro-RNAs in rodent liver are refractory to dioxin treatment. Toxicological Sciences May, 2007. Keywords: miRNA expression, response to xenobiotics, genetic modification, comparative genome hybridization In the dioxin-sensitive L-E rats we compared miRNA expression levels 19 h post-TCDD treatment vs. corn oil vehicle treatment. In the dioxin-resistant H/W rats we compared miRNA levels 19 h post-TCDD treatment vs.corn oil vehicle treatment.
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