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NASH time course study (Ldlr-/- mice on reference or Western diet)

ABSTRACT: NASH time course study (Ldlr-/- mice on reference or Western diet)

PROVIDER: PRJNA925195 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23112600.fastq.gz	Fastqsanger.gz
	SRR23112700.fastq.gz	Fastqsanger.gz
	SRR23112800.fastq.gz	Fastqsanger.gz
	SRR23112900.fastq.gz	Fastqsanger.gz
	SRR23112601.fastq.gz	Fastqsanger.gz

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NASH time course study (Ldlr-/- mice on reference or Western diet)

Project description:Mice on a reference (RD) or western diet (WD)

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NASH treatment study (Ldlr-/- mice on Western diet treated with/without omega-3 fatty acids)

Project description:NASH treatment study (Ldlr-/- mice on Western diet treated with/without omega-3 fatty acids)

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NASH prevention study (Ldlr-/- mice on Western diet treated with/without omega-3 fatty acids)

Project description:NASH prevention study (Ldlr-/- mice on Western diet treated with/without omega-3 fatty acids)

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Time course of western diet (WD) induced nonalcoholic steatohepatitis (NASH) in female and male Ldlr-/- mice.

Project description:BackgroundNonalcoholic fatty liver disease (NAFLD) is a global health problem. Identification of factors contributing to the onset and progression of NAFLD have the potential to direct novel strategies to combat NAFLD.MethodsWe examined the time course of western diet (WD)-induced NAFLD and its progression to nonalcoholic steatohepatitis (NASH) in age-matched female and male Ldlr-/- mice, with time-points at 1, 4, 8, 20 and 40 weeks on the WD. Controls included Ldlr-/- mice maintained on a purified low-fat diet (LFD) for 1 and 40 weeks. The approach included quantitation of anthropometric, plasma and liver markers of disease, plus hepatic histology, lipids, oxylipins, gene expression and selected metabolites.ResultsOne week of feeding the WD caused a significant reduction in hepatic essential fatty acids (EFAs: 18:2, ω6, 18:3, ω3) which preceded the decline in many C20-22 ω3 and ω6 polyunsaturated fatty acids (PUFA) and PUFA-derived oxylipins after 4 weeks on the WD. In addition, expression of hepatic inflammation markers (CD40, CD44, Mcp1, Nlrp3, TLR2, TLR4, Trem2) increased significantly in both female & male mice after one week on the WD. These markers continued to increase over the 40-week WD feeding study. WD effects on hepatic EFA and inflammation preceded all significant WD-induced changes in body weight, insulin resistance (HOMA-IR), oxidative stress status (GSH/GSSG ratio) and histological and gene expression markers of macrosteatosis, extracellular matrix remodeling and fibrosis.ConclusionsOur findings establish that feeding Ldlr-/- mice the WD rapidly lowered hepatic EFAs and induced key inflammatory markers linked to NASH. Since EFAs have an established role in inflammation and hepatic inflammation plays a major role in NASH, we suggest that early clinical assessment of EFA status and correcting EFA deficiencies may be useful in reducing NASH severity.

| S-EPMC10566735 | biostudies-literature

NASH treatment study (Ldlr-/- mice on Western diet treated with/without omega-3 fatty acids)

Project description:Mice on a reference (RD) or western diet (WD) supplemented with olive oil or the omega-3 fatty acid docosahexaenoic acid DHA

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Translational characterization of the temporal dynamics of metabolic dysfunctions in liver, adipose tissue and the gut during diet-induced NASH development in Ldlr−/−.Leiden mice

Project description:Title: White adipose tissue inflammation and gut permeability develop prior to NASH development, associated with increased oxidative stress, intrahepatic diacylglycerol and proinflammatory chemokines in the liver of diet-induced obese and hyperinsulinemic Ldlr-/-.Leiden mice Abstract: NAFLD progression from simple steatosis to NASH and fibrosis is driven by an intricate interplay between molecular and cellular mechanisms. These drivers are not limited to the liver itself but also white adipose tissue and gut may contribute. Current knowledge on these drivers is mostly based on studies that investigate these at a single time point (typically end-stage disease). However, such studies provide no insight into the temporal dynamics and chronology, which therefore remain poorly understood. Ldlr-/-.Leiden mice were fed a high-fat diet (HFD) to induce obesity-associated NAFLD and compared to lean controls fed chow. Groups of mice were sacrificed after 8, 16, 28 and 38 weeks to study liver, white adipose tissue, gut and circulating factors to investigate the sequence of pathogenic events in these critical metabolically active organs as well as organ-crosstalk during NAFLD development. Ldlr-/-.Leiden mice on a HFD develop obesity, dyslipidemia and insulin resistance, essentially as observed in obese NASH patients, in this translational context WAT and gut dysfunction precede the development of NASH and liver fibrosis.

2023-03-20 | GSE209762 | GEO

NASH prevention study (Ldlr-/- mice on Western diet treated with/without omega-3 fatty acids)

Project description:Mice on a reference (RD) or western diet (WD) supplemented with olive oil or omega-3 fatty acids (eicosapentaenoic acid [EPA] and/or docosahexaenoic acid [DHA])

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The effects of myeloid-specific Lipa overexpression on the transcriptomic profile of aortic plaque macrophages in mice on the Ldlr-/- background and fed a Western diet for 16 weeks

Project description:We analyzed the transcriptomic profile of aortic macrophages directly sorted from atherosclerotic aortas of two groups of mice fed a Western diet for 16 weeks: (1) mice with LysMCre-mediated myeliod-specific Lipa overexpression on the Ldlr-/- background; (2) LysMCre-negative littermates on the Ldlr-/- background.

2025-08-01 | GSE285961 | GEO

The synergestic effects of western diet and carbon tetrachloride (CCl4) to develop non-alcoholic steatohepatitis (NASH) and liver tumor in mice

Project description:NASH is a combination of hepatic steatosis and severe inflammation, which can lead to fatal liver disease such as cirrhosis and hepatocellular carcinoma. While a variety of models have been descirbed, they have several limitations. Therefore, it is of urgent importance to create animal model that recapitulate the physiology, histology and outcome seen in human with NASH. We created western diet-fed and CCl4-treated mouse model. they showed characteristic histological features of NASH such as fibrosis, ballooning and steatosis at 12 weeks and liver cancers developed at 24 weeks. Their transcritomic changes were also similar to those seen in human NASH.

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