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DICER is downregulated in mouse adipose tissue during high-fat diet feeding

ABSTRACT: DICER is downregulated in mouse adipose tissue during high-fat diet feeding

PROVIDER: PRJNA1070687 | ENA |

REPOSITORIES: ENA

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DICER is downregulated in mouse adipose tissue during high-fat diet feeding

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.

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Project description:Effect of high fat diet feeding on adipose tissue macrophages

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Genome-wide analysis of gene expression in adipose tissue of female mice after continuous high fat diet feeding

Project description:Analysis of gene expression in adipose tissue of female mice after continuous high fat diet (HFD) feeding for three generations. The hypothesis in this study is that continuous HFD feeding has transgenerational amplification effects to the offspring. Results provide important information on the impacts of over-nutrition over one generation on the offspring, such as transgenerational up-regulated or down-regulated genes.

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Fat transcriptome patterns associated with heterogeneous metabolic, hormonal and behavioral adaptation to high fat diet feeding in mice

Project description:The effect of high fat diet feeding on adipose tissue gene transcription regulation was investigated in C57Bl/6J mice using Affymetrix gene expression arrays. Expression profiling was determined in 5 months old male mice showing heterogeneous metabolic, hormonal and behavioral adaptation to high fat diet (40% fat) feeding for 15 weeks. Control mice were fed a standard carbohydrate chow. Six animals per group were used.

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Genome-wide analysis of gene expression in adipose tissue of female mice after continuous high fat diet feeding

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Mouse adipose tissue under hypercaloric and isocaloric high-fat diet

Project description:The objective of the experiment was to dissect the effects of a high-fat diet on juvenile adipose tissue gene expression under conditions of excess calorie intake versus normal calorie intake in comparison to a standard low-fat diet. For this purpose juvenile mice were fed (A) a standard low-fat diet (CD), (B) a high-fat diet ad libitum (excess calorie intake) (HFD) and (C) a high-fat diet with calorie consumption restricted to the calorie consumption of the CD diet (R-HFD). RNA expression was profiled after 1 week of feeding in the periuterine fat depot.

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Mouse muscle mitochondrial proteome changes in high fat diet vs. low fat diet

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Project description:Despite wide efforts in the last decade, signaling aberrations associated with obesity remain enigmatic. Here, we carried out phosphoproteomic analysis of mouse white adipose tissues (WAT) upon low-fat diet (LFD) and high-fat diet (HFD) to dissect underlying molecular mechanisms of obesity. Of the 7696 phosphopeptides quantified, 191 proteins including various insulin-responsive proteins and metabolic enzymes functioning in lipid homeostasis, exhibited differential phosphorylation with high-fat feeding. Kinase predictions and integrated network analysis identified several deregulated kinase signaling pathways, and suggested possibilities of HFD-induced transcriptional rewiring. Further, functional validation of a novel HFD-responsive site on cytoplasmic acetyl-coA forming ACSS2 (S263) suggested that the phosphorylation is important in regulating insulin signaling and maintaining triglyceride levels. This study represents one of the first comprehensive phosphoproteome data in mouse obesity models, and describes a systems-level approach for identifying deregulated molecular events and potential therapeutic targets in the context of high-fat feeding and adipocyte perturbation.

2016-05-20 | PXD002927 | Pride

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