High fat effect on mouse intestinal stem cells
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ABSTRACT:
PROVIDER: PRJNA636084 | ENA |
REPOSITORIES: ENA
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Project description:Examination of transcriptomic profiles of intestinal stem cells fed with different diets
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Project description:High fat diets (HFDs) are linked to several diseases including obesity, diabetes, insulin resistance, fatty liver, and susceptibility to inflammatory bowel disease (IBD) in both mouse and humans. RNA-seq from male mice (C57BL/6N) fed Vivarium Chow (VIV) or any one of three high fat diets (40% kcal fat) (SO+CO, PL+CO, CO) for 24 weeks was performed on four segments of the intestinal tract (Duodenum, Jejunum, Terminal Ileum and Proximal Colon).
2023-03-01 | GSE220302 | GEO
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:Timecourse analysis of the effect high fat and low fat diets have on liver gene expression. C57 and AJ strains examined at 0, 1, 3, 4, 5 ,6, 7, 8, 9, 10 and 11 weeks. Keywords: other
2004-07-31 | GSE536 | GEO
Project description:Research findings of the past decade have highlighted the gut as the main site of action of the oral antihyperglycemic agent metformin despite its pharmacological role in the liver. Extensive evidence supports metformin’s modulatory effect on the composition and function of gut microbiota, nevertheless, the underlying mechanisms of the host responses remain elusive. Our study aimed to evaluate metformin-induced alterations in the intestinal transcriptome profiles at different metabolic states. The high-fat diet-induced type 2 diabetes mouse model of both sexes was developed in a randomized block experiment and bulk RNA-Seq of the ileum tissue was the method of choice for comparative transcriptional profiling after metformin intervention for ten weeks. We found a prominent transcriptional effect of the diet itself with comparatively fewer genes responding to metformin intervention. The overrepresentation of immune-related genes was observed, including pronounced metformin-induced upregulation of immunoglobulin heavy-chain variable regioncoding Ighv1-7 gene in both high-fat diet and control diet-fed animals, supporting the contribution of intestinal immunoglobulin responses. Finally, we provide evidence of the downregulation NF-kappa B signaling pathway in the small intestine of both hyperglycemic and normoglycemic animals after metformin treatment. Moreover, our data pinpoint the gut microbiota as a crucial component in the metformin-mediated downregulation of NF-kappaB signaling evidenced by a positive correlation between the Rel and Rela gene expression levels and abundances of Parabacteroides distasonis, Bacteroides spp., and Lactobacillus spp. in the gut microbiota of the same animals.
2023-08-12 | GSE240206 | GEO
Project description:To further investigate the effect of high-fat diet on m6A modified expression profiles of mouse sperm RNA, we used whole-genome microarray expression profiles as a discovery platform to identify differential m6A modified genes under high-fat diet exposure. Male mice were fed normal chow (C) or 60% high-fat diet (HFD) from 5 weeks to 15 weeks old, and then sperm were obtained for Arraystar m6A-mRNA&lncRNA Epitranscriptomic Microarray. Results showed that hyper-methylated mRNAs were involved in multiple biological processes, including the "reproductive process," "gamete generation," and "spermatogenesis".
2023-12-22 | GSE241195 | GEO
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:Early nutritional environment affects development and long-term health. Our objective was to determine the effect of maternal high fat diet (HFD) during pregnancy and lactation on neonate`s duodenum histomorphology and proteome. Female mice were fed either a control diet (10% kcal fat; C) or a HFD (60% kcal fat) for four weeks, and bred. On postnatal day 2, litters were standardized to ten pups and half the pups were cross-fostered to dams fed on different diets, creating four treatment combinations: C-C (control), C-HF, HF-C, HF-HF. On postnatal day 12, pups` duodenum were excised and prepared for histology and LC-MS/MS analysis of proteome. Villi were significantly longer in duodenum of HF-HF pups compared to all other treatments. However, crypt cell proliferation rate was not different among treatments. Over 3000 proteins were detected, with 1054 commonly expressed across all groups. Between control and HF-HF, HF-C or C-HF, 812, 601 or 894 proteins were differentially expressed (Tukey adj-P <0.05), respectively. Functional analysis clustered proteins upregulated in HF-HF versus control in fat digestion and absorption, extracellular matrix, cell adhesion, immune response, oxidation-reduction processes, phagocytosis and transport categories. Proteins downregulated were classified as RNA splicing, translation, protein folding, endocytosis and transport. Thus the effect of nutritional environment on intestinal tract structure and function is manifested as early as postnatal day 12. In particular, exposure to maternal HFD during pregnancy and lactation changed fat digestion and absorption processes, increased extracellular matrix and focal adhesion proteins, and heightened innate and active immune response.
2018-08-28 | MSV000082860 | MassIVE