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High fat effect on mouse intestinal stem cells

ABSTRACT: High fat effect on mouse intestinal stem cells

PROVIDER: PRJNA636084 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11881200.fastq.gz	Fastqsanger.gz
	SRR11881201.fastq.gz	Fastqsanger.gz
	SRR11881202.fastq.gz	Fastqsanger.gz
	SRR11881203.fastq.gz	Fastqsanger.gz
	SRR11881192.fastq.gz	Fastqsanger.gz

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High fat effect on mouse intestinal stem cells

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High-fat diet enhances stemness and tumorigenicity of intestinal progenitors

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.

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High fat diet mice intestinal epithelial exosomal proteins were analyzed by MSMS.

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.

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Impact of various high fat diets on intestinal gene expression in mouse

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Reversible dietary effect on intestinal stem cells

Project description:Reversible dietary effect on intestinal stem cells

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Maternal high fat diet during gestation and lactation significantly impacts neonate intestinal morphology and proteome.

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

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