Effect of methionine/choline-deficient diet and high-fat diet-induced steatohepatitis on mitochondrial homeostasis in mice

Arao, Yoshihisa; Kawai, Hirokazu; Kamimura, Kenya; Kobayashi, Takamasa; Nakano, Oki; Hayatsu, Manabu; Ushiki, Tatsuo; Terai, Shuji

doi:10.1016/j.bbrc.2020.03.180

Cited by 20 publications

(16 citation statements)

References 13 publications

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“…Choline can be converted by the gut microbiota into trimethylamine (TMA) directly or via betaine, and TMA is oxidized into trimethylamine N-oxide (TMAO). In NAFLD, the conversion of choline into TMA/TMAO are increased, leading to deficiency of choline and accumulation of TMA/TMAO [ 64 , 65 ]. Choline can promote very low-density lipoprotein transportation out of the liver and deficiency of choline results in accumulation of lipids in the liver.…”

Section: Gut Microbiota Metabolites In the Pathogenesis Of Nafldmentioning

confidence: 99%

“…In animal models, the deficiency of choline has been shown to cause NAFLD. Arao et al (2020) used a methionine/choline-deficient diet to establish a NASH model and found that mitochondrial DNA content was decreased [ 64 ]. Hernandez et al (2020) reported that high fructose-, fat- and cholesterol feeding in pigs caused hepatic steatosis and inflammation, with impaired FXR-FGF19 signaling [ 65 ].…”

Section: Gut Microbiota Metabolites In the Pathogenesis Of Nafldmentioning

confidence: 99%

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Gut Microbiota Metabolites in NAFLD Pathogenesis and Therapeutic Implications

Chen¹,

Vitetta

2020

IJMS

197

137

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Gut microbiota dysregulation plays a key role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) through its metabolites. Therefore, the restoration of the gut microbiota and supplementation with commensal bacterial metabolites can be of therapeutic benefit against the disease. In this review, we summarize the roles of various bacterial metabolites in the pathogenesis of NAFLD and their therapeutic implications. The gut microbiota dysregulation is a feature of NAFLD, and the signatures of gut microbiota are associated with the severity of the disease through altered bacterial metabolites. Disturbance of bile acid metabolism leads to underactivation of bile acid receptors FXR and TGR5, causal for decreased energy expenditure, increased lipogenesis, increased bile acid synthesis and increased macrophage activity. Decreased production of butyrate results in increased intestinal inflammation, increased gut permeability, endotoxemia and systemic inflammation. Dysregulation of amino acids and choline also contributes to lipid accumulation and to a chronic inflammatory status. In some NAFLD patients, overproduction of ethanol produced by bacteria is responsible for hepatic inflammation. Many approaches including probiotics, prebiotics, synbiotics, faecal microbiome transplantation and a fasting-mimicking diet have been applied to restore the gut microbiota for the improvement of NAFLD.

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Section: Gut Microbiota Metabolites In the Pathogenesis Of Nafldmentioning

confidence: 99%

Section: Gut Microbiota Metabolites In the Pathogenesis Of Nafldmentioning

confidence: 99%

Gut Microbiota Metabolites in NAFLD Pathogenesis and Therapeutic Implications

Chen¹,

Vitetta

2020

IJMS

197

137

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“…Moreover, mice fed a methionine choline-deficient (MCD) diet consistently lose weight and can develop hypoglycemia [233,245]. Finally, it should be mentioned that numerous types of energydense diets can be used to induce obesity associated with simple fatty liver or NASH, but the degree of the different histopathological lesions can greatly vary between diets [241,242,246].…”

Section: Implications Of Dili In Clinical Contextsmentioning

confidence: 99%

Advanced preclinical models for evaluation of drug-induced liver injury – consensus statement by the European Drug-Induced Liver Injury Network [PRO-EURO-DILI-NET]

Fernández-Checa

Bagnaninchi

et al. 2021

Journal of Hepatology

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…TMAO exacerbates impaired glucose tolerance, obstructs hepatic insulin signaling, and promotes adipose tissue inflammation in mice maintained on a high-fat, high-sugar diet [ 106 ]. In NAFLD, the conversion of choline into TMA/TMAO is increased; thus, choline deficiency and TMA/TMAO accumulation occur [ 107 , 108 ]. Choline can induce very low-density lipoprotein transportation out of the liver; therefore, choline deficiency leads to the accumulation of lipids in the liver.…”

Section: Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

Role of Microbiota-Derived Metabolites in Alcoholic and Non-Alcoholic Fatty Liver Diseases

Park

Kim

Lee

et al. 2021

IJMS

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Chronic liver disease encompasses diseases that have various causes, such as alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). Gut microbiota dysregulation plays a key role in the pathogenesis of ALD and NAFLD through the gut–liver axis. The gut microbiota consists of various microorganisms that play a role in maintaining the homeostasis of the host and release a wide number of metabolites, including short-chain fatty acids (SCFAs), peptides, and hormones, continually shaping the host’s immunity and metabolism. The integrity of the intestinal mucosal and vascular barriers is crucial to protect liver cells from exposure to harmful metabolites and pathogen-associated molecular pattern molecules. Dysbiosis and increased intestinal permeability may allow the liver to be exposed to abundant harmful metabolites that promote liver inflammation and fibrosis. In this review, we introduce the metabolites and components derived from the gut microbiota and discuss their pathologic effect in the liver alongside recent advances in molecular-based therapeutics and novel mechanistic findings associated with the gut–liver axis in ALD and NAFLD.

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Effect of methionine/choline-deficient diet and high-fat diet-induced steatohepatitis on mitochondrial homeostasis in mice

Cited by 20 publications

References 13 publications

Gut Microbiota Metabolites in NAFLD Pathogenesis and Therapeutic Implications

Gut Microbiota Metabolites in NAFLD Pathogenesis and Therapeutic Implications

Advanced preclinical models for evaluation of drug-induced liver injury – consensus statement by the European Drug-Induced Liver Injury Network [PRO-EURO-DILI-NET]

Role of Microbiota-Derived Metabolites in Alcoholic and Non-Alcoholic Fatty Liver Diseases

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