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Effect of methionine-chorine-deficient diet (MCD) in murine liver

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): synthetic construct Mus musculus

PROVIDER: GSE249487 | GEO | 2023/12/06

REPOSITORIES: GEO

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Effect of methionine-chorine-deficient diet (MCD) on microRNA expression in murine liver [miRNA]

Project description:It is known that administration of MCD induces a severe state of hepatic fibrosis in mice. Recently, many microRNAs (miRNAs) with pro- or anti-fibrotic properties have been identified during hepatic fibrosis. To attempt to elucidate molecular mechanism of hepatic fibrosis involved in miRNA fnction, we performed comprehensive analysis of miRNA expression by microarray using RNAs prepared from liver of wild-type mice fed with normal diet (ND) or MCD.

2023-12-06 | GSE249486 | GEO

Effect of methionine-chorine-deficient diet (MCD) in murine liver

Project description:Effect of methionine-chorine-deficient diet (MCD) in murine liver

| PRJNA1049364 | ENA

Effect of methionine-chorine-deficient diet (MCD) on whole gene expression in murine liver [mRNA]

Project description:It is known that administration of MCD induces a severe state of hepatic fibrosis in mice. To attempt to elucidate molecular mechanism of hepatic fibrosis, we performed whole transcriptome analysis by microarray using RNAs prepared from liver of wild-type mice fed with normal diet (ND) or MCD.

2023-12-06 | GSE249485 | GEO

Effect of methionine-chorine-deficient diet (MCD) on microRNA expression in murine liver [miRNA]

Project description:Effect of methionine-chorine-deficient diet (MCD) on microRNA expression in murine liver [miRNA]

| PRJNA1049370 | ENA

Effect of methionine-chorine-deficient diet (MCD) on whole gene expression in murine liver [mRNA]

Project description:Effect of methionine-chorine-deficient diet (MCD) on whole gene expression in murine liver [mRNA]

| PRJNA1049371 | ENA

A CD209 ligand and a sialidase inhibitor differentially modulate adipose tissue and liver macrophage populations and steatosis in mice on the Methionine and Choline-Deficient (MCD) diet.

Project description:Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and type 2 diabetes and is characterized by the accumulation of fat in the liver (steatosis). NAFLD can transition into non-alcoholic steatohepatitis (NASH), with liver cell injury, inflammation, and an increased risk of fibrosis. We previously found that injections of either 1866, a synthetic ligand for the lectin receptor CD209, or DANA, a sialidase inhibitor, can inhibit inflammation and fibrosis in multiple animal models. The methionine and choline-deficient (MCD) diet is a model of NASH which results in the rapid induction of liver steatosis and inflammation. In this report, we show that for C57BL/6 mice on a MCD diet, injections of both 1866 and DANA reversed MCD diet-induced decreases in white fat, decreases in adipocyte size, and white fat inflammation. However, these effects were not observed in type 2 diabetic db/db mice on a MCD diet. In db/db mice on a MCD diet, 1866 decreased liver steatosis, but these effects were not observed in C57BL/6 mice. There was no correlation between the ability of 1866 or DANA to affect steatosis and the effects of these compounds on the density of liver macrophage cells expressing CLEC4F, CD64, F4/80, or Mac2. Together these results indicate that 1866 and DANA modulate adipocyte size and adipose tissue macrophage populations, that 1866 could be useful for modulating steatosis, and that changes in the local density of 4 different liver macrophages cell types do not correlate with effects on liver steatosis.

| S-EPMC7773271 | biostudies-literature

DNMT1 KNOCKOUT IN MURINE LIVER

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-04-01 | E-GEOD-67771 | biostudies-arrayexpress

Stress signaling in the methionine-choline-deficient model of murine fatty liver disease.

Project description:Stress signaling, both within and outside the endoplasmic reticulum, has been linked to metabolic dysregulation and hepatic steatosis. Methionine-choline-deficient (MCD) diets cause severe fatty liver disease and have the potential to cause many types of cellular stress. The purpose of this study was to characterize hepatic stress in MCD-fed mice and explore the relationship between MCD-mediated stress and liver injury.Stress signaling was examined in mice fed MCD formulas for 4-21 days. Signaling also was evaluated in mice fed MCD formulas supplemented with clofibrate, which inhibits hepatic triglyceride accumulation. The role of the pro-apoptotic stress protein C/EBP homologous protein (CHOP) in MCD-mediated liver injury was assessed by comparing the responses of wild-type and CHOP-deficient mice to an MCD diet.MCD feeding caused steatohepatitis coincident with the activation of cJun N-terminal kinase and caspase-12. In contrast, MCD feeding did not activate inositol-requiring protein-1 and actually suppressed the expression of X-box protein-1s. MCD feeding caused weak stimulation of double-stranded RNA-activated protein kinase-like endoplasmic reticulum-resident kinase, but robust activation of general control nonderepressible-2, followed by the phosphorylation of eukaryotic initiating factor-2? and induction of CHOP. Clofibrate eliminated MCD-mediated hepatic steatosis but did not inhibit diet-induced stress. CHOP deficiency did not alleviate, and in fact worsened, MCD-mediated liver disease.MCD feeding causes an integrated stress response in the liver rather than a classic unfolded protein response. This stress response does not by itself lead to liver injury. CHOP, despite its identity as a mediator of stress-related cell death, does not play a central role in the pathogenesis of MCD-mediated liver disease.

| S-EPMC2967598 | biostudies-literature

MCD diet-induced steatohepatitis generates a diurnal rhythm of associated biomarkers and worsens liver injury in Klf10 deficient mice.

Project description:A large number of hepatic functions are regulated by the circadian clock and recent evidence suggests that clock disruption could be a risk factor for liver complications. The circadian transcription factor Krüppel like factor 10 (KLF10) has been involved in liver metabolism as well as cellular inflammatory and death pathways. Here, we show that hepatic steatosis and inflammation display diurnal rhythmicity in mice developing steatohepatitis upon feeding with a methionine and choline deficient diet (MCDD). Core clock gene mRNA oscillations remained mostly unaffected but rhythmic Klf10 expression was abolished in this model. We further show that Klf10 deficient mice display enhanced liver injury and fibrosis priming upon MCDD challenge. Silencing Klf10 also sensitized primary hepatocytes to apoptosis along with increased caspase 3 activation in response to TNFα. This data suggests that MCDD induced steatohepatitis barely affects the core clock mechanism but leads to a reprogramming of circadian gene expression in the liver in analogy to what is observed in other experimental disease paradigms. We further identify KLF10 as a component of this transcriptional reprogramming and a novel hepato-protective factor.

| S-EPMC7376252 | biostudies-literature

Effect of methionine/choline deficient diet on liver and suprachiasmatic nucleus circadian transcriptome.

Project description:The feeding/fasting cycles controlled by our circadian clock impose great daily metabolic and physiological changes, and yet investigations into the consequences of metabolic deficiencies, either dietary or genetic, have often ignored the time of day or the circadian time of the animals or subjects. In addition, these deficiencies may themselves disrupt our circadian clock, causing secondary metabolic, physiological and behavioural disorders. Dietary methionine/choline deficiency in rodents is a common model for human non-alcoholic steatohepatitis, but methionine and choline are nutrients essential for many other processes beyond fatty acid synthesis in the liver, including biological methylations and 1-carbon metabolism, regulation of translation notably via the mTOR pathway, phospholipid synthesis, polyamine pathway and glutathione synthesis. We have previously shown that circadian rhythms in many organisms are highly sensitive to deficiency or excesses of 1-carbon metabolites. Using a methionine/choline deficient diet in mice, we illustrate the nutrigenomic crosstalk between circadian rhythms and 1-carbon metabolism. We show not only that circadian locomotor activity behaviour is profoundly, rapidly and reversibly affected by methionine/choline deficiency, but also that the effects of methionine/choline deficiency on gene expression and 1-carbon metabolites are dependent on circadian time, illustrating the importance of considering circadian rhythms in metabolic studies. This study also highlights the impact of what we eat, or don't, on our behaviour and biological rhythms.

2024-01-05 | GSE252364 | GEO

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