Micronutrient Antioxidants and Nonalcoholic Fatty Liver Disease

Chen, Guanliang; Ota, Tsuguhito; Nagata, Naoto; Xu, Liang

doi:10.3390/ijms17091379

Cited by 59 publications

(58 citation statements)

References 141 publications

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“…[110] AX is a xanthophyll carotenoid that is recognized as a novel antioxidant preventing cardiovascular and liver diseases. [112] We previously found that AX decreases fat accumulation and peroxidation in diet-induced NASH mice and primary hepatocytes. [111] We also reported that lycopene ameliorates diet-induced fatty liver and hepatic inflammation in the mice fed with HFD or CL diet by promoting M2-dominant polarization in adipose tissue, suggesting its potential role in the treatment of liver diseases.…”

Section: Micronutrient Antioxidantsmentioning

confidence: 94%

The Gut Microbiota and Its Metabolites, Novel Targets for Treating and Preventing Non‐Alcoholic Fatty Liver Disease

Ota

Zhuge

et al. 2020

Molecular Nutrition Food Res

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Non‐alcoholic fatty liver disease (NAFLD) is one of the most prevalent metabolic disorders worldwide, along with obesity and type 2 diabetes. NAFLD involves a series of liver abnormalities from simple hepatic steatosis to non‐alcoholic steatohepatitis, which can ultimately lead to liver cirrhosis and cancer. The gut–liver axis plays an important role in the development of NAFLD, which depends mainly on regulation of the gut microbiota and its bacterial products. These intestinal bacterial species and their metabolites, including bile acids, tryptophan catabolites, and branched‐chain amino acids, regulate adipose tissue and intestinal homeostasis and contribute to the pathogenesis of NAFLD/non‐alcoholic steatohepatitis. In this review, the current evidence regarding the key role of the gut microbiota and its metabolites in the pathogenesis and development of NAFLD is highlighted, and the advances in the progression and applied prospects of gut microbiota‐targeted dietary and exercise therapies is also discussed.

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Section: Micronutrient Antioxidantsmentioning

confidence: 94%

The Gut Microbiota and Its Metabolites, Novel Targets for Treating and Preventing Non‐Alcoholic Fatty Liver Disease

Ota

Zhuge

et al. 2020

Molecular Nutrition Food Res

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“…As with vitamin E, astaxanthin significantly reduced the levels of the oxidative stress marker thiobarbituric acid reactive substances (TBARS) in the livers of mice with NASH [14]. Vitamin E has been used as a therapeutic component for NAFLD through its inhibition of reactive oxygen species production [13]. Our results suggested that vitamin E effectively reduced ER stress and improved EIF2 protein translation.…”

Section: Discussionmentioning

confidence: 86%

“…A meta-analysis of randomized controlled trials concluded that supplementation with astaxanthin had a slight plasma glucose-lowering effect [10]. Recently, astaxanthin’s protective effect on liver function has been attracting attention [9,11,12,13]. We have previously shown that astaxanthin ameliorated hepatic steatosis in both ob/ob and high-fat-diet-induced obese mice [14].…”

Section: Introductionmentioning

confidence: 99%

Hepatic Transcriptome Profiles of Mice with Diet-Induced Nonalcoholic Steatohepatitis Treated with Astaxanthin and Vitamin E

Kobori

Takahashi

Sakurai

et al. 2017

IJMS

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Astaxanthin alleviates hepatic lipid accumulation and peroxidation, inflammation, and fibrosis in mice with high-cholesterol, high-cholate, and high-fat (CL) diet-induced nonalcoholic steatohepatitis (NASH). It has been proposed as a potential new treatment to inhibit the progression of NASH in humans. In this study, we compared hepatic gene expression profiles after treatment with astaxanthin or the antioxidant vitamin E in mice with CL diet-induced NASH. Comprehensive gene expression analyses of the livers of mice fed a standard, CL, or CL diet containing astaxanthin or vitamin E for 12 weeks were performed using a DNA microarray. Both astaxanthin and vitamin E effectively improved gene expression associated with eukaryotic initiation factor-2 (EIF2) signaling, which is suppressed in NASH by endoplasmic reticulum (ER) stress in the liver. However, astaxanthin did not improve the expression of genes associated with mitochondrial dysfunction. Astaxanthin, but not vitamin E, was predicted to suppress the actions of ligand-dependent nuclear receptors peroxisome proliferator-activated receptors, (PPAR) α (PPARA) and PPARδ (PPARD), and to affect related molecules. Establishing a new therapy using astaxanthin will require elucidation of astaxanthin's molecular action on the functions of PPARα and related molecules in the livers of mice with diet-induced NASH.

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“…It has been informed that EGC enriched LSE as an anti-inflammatory agent in Lipopolysaccharides-stimulated HepG2 cells and mice [25]. Recent evidences have focused on the control for NAFLD pathogenesis using micronutrient antioxidants and/or dietary components, such as vitamins and polyphenols [41][42][43]. In the literature, polyphenols are a heterogeneous class of plant-derived compounds, with some confirmed hepatoprotective effects [44].…”

Section: Discussionmentioning

confidence: 99%

Lotus Seedpod Extracts Reduced Lipid Accumulation and Lipotoxicity in Hepatocytes

et al. 2019

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Non-alcoholic fatty liver disease (NAFLD) is closely associated with metabolic disorders, including hepatic lipid accumulation and lipotoxicity. Plant-derived polyphenols have attracted considerable attention in the prevention of NAFLD. Lotus seedpod, rich in polyphenols, is a traditional Chinese herbal medicine. Previous studies have showed that lotus seedpod possess radioprotective, antioxidant, anti-cancer, and anti-inflammatory activities. In this study, the in vitro hepatoprotective effect of lotus seedpod extract (LSE) and its main component epigallocatechin (EGC) was examined. Firstly, oleic acid (OA), an unsaturated fatty acid, was used to induce the phenotype of NAFLD in human hepatocytes, HepG2 cells. LSE dose-dependently improved the OA-induced viability loss of HepG2 cells. Non-cytotoxic concentrations of LSE or EGC abolished intracellular lipid accumulation and oxidative stress in the OA-treated cells. In addition, LSE and EGC showed a minor effect on autophagy, and potential in reducing OA-induced occurrence of apoptosis confirmed by morphological and biochemical features, including an increase in the formation of apoptotic bodies, the exposure of phosphatidylserine, and activation of caspases. Molecular data showed the anti-apoptotic effect of LSE might be mediated via downregulation of the mitochondrial pathway. Our data imply that EGC-enriched LSE potentially could be developed as an anti-NAFLD agent.

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Micronutrient Antioxidants and Nonalcoholic Fatty Liver Disease

Cited by 59 publications

References 141 publications

The Gut Microbiota and Its Metabolites, Novel Targets for Treating and Preventing Non‐Alcoholic Fatty Liver Disease

The Gut Microbiota and Its Metabolites, Novel Targets for Treating and Preventing Non‐Alcoholic Fatty Liver Disease

Hepatic Transcriptome Profiles of Mice with Diet-Induced Nonalcoholic Steatohepatitis Treated with Astaxanthin and Vitamin E

Lotus Seedpod Extracts Reduced Lipid Accumulation and Lipotoxicity in Hepatocytes

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