Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA229383 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiles of intestinal CD4 T-cells from control, HFD-induced prediabetic and diabetic mice
| PRJNA229384 | ENA
Project description:High-fat diet (HFD) decreases insulin sensitivity. How high-fat diet causes insulin resistance is largely unknown. Here, we show that lean mice become insulin resistant after being administered exosomes isolated from the feces of obese mice fed a high-fat diet (HFD) or from human type II diabetic patients with diabetes. HFD altered the lipid composition of exosomes from predominantly PE in exosomes from lean animals (L-Exo) to PC in exosomes from obese animals (H-Exo). Mechanistically, we show that intestinal H-Exo is taken up by macrophages and hepatocytes, leading to inhibition of the insulin signaling pathway. Moreover, exosome-derived PC binds to and activates AhR, leading to inhibition of the expression of genes essential for activation of the insulin signaling pathway, including IRS-2, and its downstream genes PI3K and Akt. Together, our results reveal HFD-induced exosomes as potential contributors to the development of insulin resistance. Intestinal exosomes thus have potential as broad therapeutic targets.
2021-03-23 | PXD022641 | Pride
Project description:Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors. mRNA profiles of intestinal stem cells (GFP-Hi) and progenitors (GFP-Low) from WT or HFD fed mice were generated by deep sequencing using HiSeq 2000.
2016-02-16 | E-GEOD-67324 | biostudies-arrayexpress
Project description:Purpose: Aim of the study was to identify transcriptional changes in the intestinal B cells of NASH-affected mice versus healthy mice. Results: RNA-Seq analysis in both sorted CD19+/CD20+ and sorted B220+ cells, revealed increased expression levels in genes involved in lipid metabolism, and in antigen presentation, BCR signaling, B cells activation and proliferation. Conclusion: Mice bearing NASH (both WT and μMT choline-deficient high-fat diet (CD-HFD) fed mice) display altered B cells in the gastrointestinal tract towards an activated phenotype and increased proliferation induced by the CD-HFD.
2023-12-01 | GSE190691 | GEO
Project description:To determine whether diet-induced changes in gut microbiota modified intestinal immune cell gene expression, we analyzed the transcriptome of antigen presenting cells isolated from the lamina propria of the small intestine of mice fed with different diet.
2015-11-18 | GSE52557 | GEO
Project description:As early as one month of age, nonobese diabetic (NOD) mice feature pancreatic infiltration of autoreactive T lymphocytes, which destruct insulin-producing beta cells, producing autoimmune diabetes mellitus (T1D) within eightmonths. Thus, we hypothesized that during the development of T1D, the transcriptional modulation of immune reactivity genes may occur as thymocytes mature into peripheral T lymphocytes. The transcriptome of thymocytes and peripheral CD3+ T lymphocytes from prediabetic or diabetic mice analyzed through microarray hybridizations identified the differentially expressed genes.
2012-07-31 | E-MEXP-3572 | biostudies-arrayexpress
Project description:As early as one month of age, nonobese diabetic (NOD) mice feature pancreatic infiltration of autoreactive T lymphocytes, which destruct insulin-producing beta cells, producing autoimmune diabetesmellitus (T1D) within eight months. Thus, we hypothesized that during the development of T1D, the transcriptional modulation of immune reactivity genes may occur as thymocytes mature into peripheral T lymphocytes. The transcriptome of thymocytes and peripheral CD3+ T lymphocytes from prediabetic or diabetic mice analyzed through microarray hybridizations identified the differentially expressed genes.
2012-07-31 | E-MEXP-3573 | biostudies-arrayexpress
Project description:We profiled three prominent ATM subtypes from human visceral omental adipose tissue in obesity by RNA-seq. In the related manuscript, we evaluated differences in their signatures and their relationship to type 2 diabetes: Visceral (VAT) and subcutaneous (SAT) adipose tissue samples were collected from diabetic and non-diabetic obese subjects to evaluate cellular content and gene expression. VAT CD206+CD11c− ATMs were increased in diabetic subjects, scavenger receptor-rich with low intracellular lipids, secreted proinflammatory cytokines, and diverged significantly from two CD11c+ ATM subtypes, which were lipid-laden, lipid antigen presenting, and overlapped with monocyte signatures. Furthermore, diabetic VAT was enriched for CD206+CD11c− ATM and inflammatory signatures, scavenger receptors, and MHC II antigen presentation genes. VAT immunostaining found CD206+CD11c⁻ ATMs concentrated in vascularized lymphoid clusters adjacent to CD206⁻CD11c+ ATMs, while CD206+CD11c+ were distributed between adipocytes. Our results suggest ATM subtype-specific profiles that uniquely contribute to the phenotypic variation in obesity.
2022-01-31 | GSE189849 | GEO
