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Gut-liver crosstalk in MASLD + EtOH patients

ABSTRACT: SLD patients and regular daily alcohol consumption

PROVIDER: PRJEB86160 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR14758720_1.fastq.gz	Fastqsanger.gz
	ERR14758720_2.fastq.gz	Fastqsanger.gz
	ERR14758721_1.fastq.gz	Fastqsanger.gz
	ERR14758721_2.fastq.gz	Fastqsanger.gz
	ERR14758722_1.fastq.gz	Fastqsanger.gz

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Alcohol consumption in metabolic associated liver disease (MASLD)

Project description:Recently, alcohol consumption in metabolic associated steatotic liver disease (MASLD) patients is increasing its incidence. However the pathophysiological mechanisms triggering liver damage in this condition remain unclear. In the present study we aimed to elucidate liver phenotype and gut-liver crosstalk in the context of SLD induced by simultaneous and deleterious association of alcohol and metabolic risk factors.

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Alcohol consumption in metabolic associated liver disease (MASLD)

Project description:Alcohol consumption in metabolic associated liver disease (MASLD)

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Blockade of lL17 signaling reverses alcohol-induced liver injury, and excessive alcohol drinking in mice.

Project description:Chronic alcohol abuse has a detrimental effect on the brain and liver. There is no effective treatment for these patients and the mechanism underlying alcohol addiction and consequent alcohol-induced damage of the liver/brain axis remains unresolved. We compared experimental models of alcoholic liver disease (ALD) and alcohol dependence in mice and demonstrated that genetic ablation of IL17 Receptor A (IL17ra-/-), or pharmacological blockade of IL17 signaling effectively suppressed the increased voluntary alcohol drinking in alcohol-dependent mice, and blocked alcohol-induced hepatocellular and neurological damage. The level of circulating IL17A positively correlated with the alcohol use in excessive drinkers, and was further increased in patients with ALD as compared to healthy individuals. Our data suggest that IL17A is a common mediator of excessive alcohol consumption and alcohol-induced liver/brain injury, and targeting IL17A may provide a novel strategy for treatment of alcohol-induced pathology.

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Targeting the Adipose Tissue-Liver-Gut Microbiota Crosstalk to Cure MASLD.

Project description: Not available

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Gene expression in brain and liver produced by three different regimens of alcohol consumption in mice: Comparison with immune activation

Project description:We investigated the molecular mechanisms of chronic alcohol consumption or lipopolysaccharide insult by gene expression profiling in prefrontal cortex and liver of C57BL/6J mice. We identified similar patterns of transcriptional changes in brain and liver among three different alcohol consumption tests and lipopolysaccharide injection. We also demonstrated distinct genomic consequences of different types of alcohol consumption. The microarray experiment was performed to compare gene expression changes induced by three separate paradigms of alcohol consumption and immune activation by lipopolysaccharide injection. The three tests of alcohol consumption were the continuous chronic two bottle choice (Chronic), two bottle choice available every other day (Chronic Intermittent) and limited access to one bottle of ethanol (Drinking in the Dark). All alcohol studies utilized 20% ethanol and each treatment group had it's own control group which received only water. The immune activation test consisted of 2 lipopolysaccharide injections (1 mg/kg i.p.) spaced one week apart, with animals being sacrificed one week after the last injection. Control animals received saline injections. All studies used female, adult mice.

2013-04-01 | E-GEOD-42789 | biostudies-arrayexpress

iPSC-Derived Hepatocytes from Patients with MASLD Exhibit Early Mitochondrial Dysfunction

Project description:iPSCs from 10 MASLD patients and 10 healthy control subjects genotyped for the I148M variant of PNPLA3 were differentiated to iPSC-Heps. Mitochondrial mass and function were assessed under basal culture conditions and following short-term exposure to exogenous palmitate. Outcomes included gene expression, mitochondrial oxygen consumption, ROS production and cellular energy status. iPSC-Heps from MASLD patients exhibited mitochondrial alterations characteristic of their diseased origin. The degree of mitochondrial dysfunction seen in MASLD iPSC-Heps was reminiscent of that described clinically in early MASLD, prior to progression to steatohepatitis. Mitochondrial alterations in MASLD iPSC-Heps occurred independently of PNPLA3 genotype.

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Project description:The mice were administered 20% edible alcohol (15 µL/g) by gavage daily for 2 weeks, while the control group was administered normal saline solution.

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Project description: Not available

| S-EPMC12016937 | biostudies-literature

Transcriptomic data from the liver of Ahr knockout mice

Project description:Alcoholic liver disease, which varies in severity from mild steatosis to cirrhosis and hepatitis, is one of the most prevalent chronic liver diseases worldwide. Excessive alcohol consumption remains the leading cause of ALD and alcohol-related complications and deaths. However, no medications have been developed to treat this disease and its pathogenesis remains elusive. Here, to understand alcohol-induced AhR activation in more detail, transcriptomic data was conducted using livers from mice subjected to either control or Lieber-DeCarli alcohol diets.

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