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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Public Health".

Deadline for manuscript submissions: closed (20 February 2022) | Viewed by 38348

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Prof. Dr. Naoki Tanaka

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Department of Global Medical Research Promotion, Shinshu University Graduate School of Medicine, Matsumoto 390-8621, Japan
Interests: non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH); nutrient metabolism; PPAR; hepatic fibrosis; hepatocarcinogenesis
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Dear Colleagues,

Homeostasis of nutrients, such as glucose, amino acid, lipid, vitamin, and trace element, is mainly regulated by liver and its disruption causes various liver disease. For instance, a high-fat high-fructose diet leads to obesity, hepatic insulin resistance, and non-alcoholic fatty liver disease, which may progress into liver cirrhosis and cancer. Protein-energy malnutrition is often detected in the patients with liver cirrhosis and branched-chain amino acid supplementation can improve the outcome of cirrhotic patients. Furthermore, dietary saturated fat, trans fat, and cholesterol may give different impact on the development of non-alcoholic steatohepatitis and liver cancer. These findings indicate a close linkage between nutrients and liver disease, and we always need to recognize the importance of nutritional aspects in the pathogenesis of liver disease. In this issue, we would like to summarize the current studies regarding nutrition and liver disease and discuss future direction of nutritional researches. We welcome many manuscripts regarding not only the association between nutrients and liver disease, but also promising dietary interventions, including fasting, calorie restriction, and functional foods.

Prof. Naoki Tanaka
Guest Editor

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Keywords

non-alcoholic fatty liver disease
non-alcoholic steatohepatitis
liver cirrhosis
liver cancer
trans fatty acid
cholesterol
fructose
branched chain amino acid
microbiota
dietary restriction
senescence
functional foods

Published Papers (11 papers)

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Research

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16 pages, 5305 KiB

Open AccessArticle

RNA-Seq Analysis of Protection against Chronic Alcohol Liver Injury by Rosa roxburghii Fruit Juice (Cili) in Mice

by Shan Yang, Xian-Yu Huang, Nian Zhou, Qin Wu, Jie Liu and Jing-Shan Shi

Nutrients 2022, 14(9), 1974; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14091974 - 09 May 2022

Cited by 7 | Viewed by 2670

Abstract

Rosa roxburghii Tratt. fruit juice (Cili) is used as a medicinal and edible resource in China due to its antioxidant and hypolipidemic potentials. The efficacy of Cili in protecting alcohol-induced liver injury and its underlying mechanism was investigated. C57BL/6J mice received a Lieber-DeCarli liquid diet containing alcohol to produce liver injury. After the mice were adapted gradually to 5% alcohol, Cili (4 mL and 8 mL/kg/day for 4 weeks) were gavaged for treatment. The serum enzyme activities, triglyceride levels, histopathology and Oil-red O staining were examined. The RNA-Seq and qPCR analyses were performed to determine the protection mechanisms. Cili decreased serum and liver triglyceride levels in mice receiving alcohol. Hepatocyte degeneration and steatosis were improved by Cili. The RNA-Seq analyses showed Cili brought the alcohol-induced aberrant gene pattern towards normal. The qPCR analysis verified that over-activation of CAR and PXR (Cyp2a4, Cyp2b10 and Abcc4) was attenuated by Cili. Cili alleviated overexpression of oxidative stress responsive genes (Hmox1, Gsta1, Gstm3, Nqo1, Gclc, Vldlr, and Cdkn1a), and rescued alcohol-downregulated metabolism genes (Angptl8, Slc10a2, Ces3b, Serpina12, C6, and Selenbp2). Overall, Cili was effective against chronic alcohol liver injury, and the mechanisms were associated with decreased oxidative stress, improved lipid metabolism through modulating nuclear receptor CAR-, PXR-and Nrf2-mediated pathways. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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14 pages, 1022 KiB

Open AccessArticle

Oral Intake of L-Ornithine-L-Aspartate Is Associated with Distinct Microbiome and Metabolome Changes in Cirrhosis

by Angela Horvath, Julia Traub, Benard Aliwa, Benjamin Bourgeois, Tobias Madl and Vanessa Stadlbauer

Nutrients 2022, 14(4), 748; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14040748 - 10 Feb 2022

Cited by 2 | Viewed by 4497

Abstract

L-ornithine L-aspartate (LOLA) is administered as a therapeutic and/or preventive strategy against hepatic encephalopathy either intravenously or orally in patients with liver cirrhosis. Here, we analyzed how LOLA influences the microbiome and metabolome of patients with liver cirrhosis. We retrospectively analyzed the stool microbiome, stool, urine and serum metabolome as well as markers for gut permeability, inflammation and muscle metabolism of 15 cirrhosis patients treated orally with LOLA for at least one month and 15 propensity-score-matched cirrhosis patients without LOLA. Results were validated by comparing the LOLA-treated patients to a second set of controls. Patients with and without LOLA were comparable in age, sex, etiology and severity of cirrhosis as well as PPI and laxative use. In the microbiome, Flavonifractor and Oscillospira were more abundant in patients treated with LOLA compared to the control group, while alpha and beta diversity were comparable between groups. Differences in stool and serum metabolomes reflected the pathophysiology of hepatic encephalopathy and confirmed LOLA intake. In the urine metabolome, ethanol to acetic acid ratio was lower in patients treated with LOLA compared to controls. LOLA-treated patients also showed lower serum levels of insulin-like growth factor (IGF) 1 than patients without LOLA. No differences in gut permeability or inflammation markers were found. A higher abundance of Flavonifractor and Oscillospira in LOLA-treated patients could indicate LOLA as a potential microbiome modulating strategy in patients with liver disease. The lower levels of IGF1 in patients treated with LOLA suggest a possible link between the pathophysiology of hepatic encephalopathy and muscle health. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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13 pages, 2664 KiB

Open AccessEditor’s ChoiceArticle

Lysophosphatidylethanolamine Affects Lipid Accumulation and Metabolism in a Human Liver-Derived Cell Line

by Yusuke Yamamoto, Toshihiro Sakurai, Zhen Chen, Nao Inoue, Hitoshi Chiba and Shu-Ping Hui

Nutrients 2022, 14(3), 579; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14030579 - 28 Jan 2022

Cited by 33 | Viewed by 4099

Abstract

The physiological functions of lysophosphatidylethanolamine (lysoPE) have not been fully elucidated. In this study, the effects of lysoPE on lipogenesis and lipolysis were investigated in a cultured human liver-derived cell line. The intracellular lipid profile was investigated in detail using liquid chromatography–tandem mass spectrometry (LC-MS/MS) to better understand the underlying mechanism. The expression of genes related to lipid metabolism and catabolism was analyzed using real-time PCR. LysoPE supplementation induced cellular lipid droplet formation and altered triacylglycerol (TAG) profiles. Furthermore, lysoPE downregulated expression of the TAG hydrolyzation regulation factor ATGL, and reduced the expression of fatty acid biosynthesis-related genes SREBP1 and SCD1. LC-MS/MS-based lipidomic profiling revealed that the addition of lysoPE 18:2 increased the PE species containing linoleic acyl, as well as the CE 18:2 species, likely due to the incorporation of linoleic acyl from lysoPE 18:2. Collectively, these findings suggest that lysoPE 18:2 is involved in lipid droplet formation by suppressing lipolysis and fatty acid biosynthesis. Thus, lysoPE might play a pathological role in the induction of fatty liver disease. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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14 pages, 2135 KiB

Open AccessArticle

A Comparative Study of the Hepatoprotective Effect of Centella asiatica Extract (CA-HE50) on Lipopolysaccharide/d-galactosamine-Induced Acute Liver Injury in C57BL/6 Mice

by Woojae Hong, Jeon Hwang-Bo, Hyelin Jeon, Minsung Ko, Joongyeon Choi, Yong-Joon Jeong, Jae-Hyun Park, Inhye Kim, Tae-Woo Kim, Hyunggun Kim and Se-Chan Kang

Nutrients 2021, 13(11), 4090; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13114090 - 15 Nov 2021

Cited by 7 | Viewed by 3079

Abstract

Acute liver failure (ALF) refers to the sudden loss of liver function and is accompanied by several complications. In a previous study, we revealed the protective effect of Centella asiatica 50% ethanol extract (CA-HE50) on acetaminophen-induced liver injury. In the present study, we investigate the hepatoprotective effect of CA-HE50 in a lipopolysaccharide/galactosamine (LPS-D-Gal)-induced ALF animal model and compare it to existing therapeutic silymarin, Lentinus edodes mycelia (LEM) extracts, ursodeoxycholic acid (UDCA) and dimethyl diphenyl bicarboxylate (DDB). Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were decreased in the CA-HE50, silymarin, LEM, UDCA and DDB groups compared to the vehicle control group. In particular, AST and ALT levels of the 200 mg/kg CA-HE50 group were significantly decreased compared to positive control groups. Lactate dehydrogenase (LDH) levels were significantly decreased in the CA-HE50, silymarin, LEM, UDCA and DDB groups compared to the vehicle control group and LDH levels of the 200 mg/kg CA-HE50 group were similar to those of the positive control groups. Superoxide dismutase (SOD) activity was significantly increased in the 100 mg/kg CA-HE50, LEM and UDCA groups compared to the vehicle control group and, in particular, the 100 mg/kg CA-HE50 group increased significantly compared to positive control groups. In addition, the histopathological lesion score was significantly decreased in the CA-HE50 and positive control groups compared with the vehicle control group and the histopathological lesion score of the 200 mg/kg CA-HE50 group was similar to that of the positive control groups. These results show that CA-HE50 has antioxidant and hepatoprotective effects at a level similar to that of silymarin, LEM, UDCA and DDB, which are known to have hepatoprotective effects; further, CA-HE50 has potential as a prophylactic and therapeutic agent in ALF. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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14 pages, 302 KiB

Open AccessArticle

Synergistic Interaction of Dietary Pattern and Concordance Lifestyle with Abnormal Liver Function among Young Adults in Taiwan: A Population-Based Longitudinal Study

by Rathi Paramastri, Chien-Yeh Hsu, Yung-Kun Chuang, Hsiu-An Lee, Bayu Satria Wiratama and Jane C.-J. Chao

Nutrients 2021, 13(10), 3591; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103591 - 14 Oct 2021

Cited by 3 | Viewed by 1994

Abstract

While diet and lifestyle are independently implicated in the etiology of liver disease, the interaction of diet and lifestyle may be more helpful for determining the risk of liver abnormality. Thus, our study aimed to evaluate the interaction between the dietary pattern associated with liver biomarkers and lifestyle factors among Taiwanese adults with abnormal liver enzymes. A liver-associated dietary pattern, generated using reduced rank regression, was characterized by high intake of soy sauce or other dips, sugar sweetened beverages, and preserved and processed foods, but low intake of seafood, fruits, eggs, and dark-colored vegetables. In the fully adjusted model, liver-associated dietary patterns or unhealthy concordance lifestyle factors were associated with an increased risk of having liver function abnormality (OR = 1.08, 95% CI: 1.04, 1.12 and OR = 1.42, 95% CI: 1.31, 1.53, respectively). Moreover, the interaction between liver-associated dietary pattern and unhealthy concordance lifestyle factors showed more significant correlation, with an elevated risk of abnormal liver function (OR = 2.14, 95% CI: 2.02, 2.26). Therefore, our study suggests that participants who have a strong liver-associated dietary pattern along with unhealthy concordance lifestyles are likely to have increased odds of abnormal liver function. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

13 pages, 2652 KiB

Open AccessArticle

Study of the Potential Hepatoprotective Effect of Myo-Inositol and Its Influence on Zebrafish Development

by Tomasz Antonowski, Karol Wiśniewski, Piotr Podlasz, Adam Osowski and Joanna Wojtkiewicz

Nutrients 2021, 13(10), 3346; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103346 - 24 Sep 2021

Cited by 2 | Viewed by 1826

Abstract

Inositol is a natural substance found widely in plants. It is used in therapies for many medical cases. The aim of this study was to determine the toxicity of myo-inositol (MI) and to investigate its potential hepatoprotective character. In the first part of the study, zebrafish embryos were incubated with 5, 10, 20, 40, 60, 80, and 100 mg/mL MI. Endpoints such as survivability, hatching rate, malformation, and mobility were evaluated. Our results demonstrated that the high doses of MI lead to increased mortality and malformations and reduce the hatching rate in comparison to the control group. Moreover, low doses of this compound do not produce a negative effect on zebrafish and even have the ability to increase the hatching rate and mobility. In the second part of the study, the hepatoprotective effect of MI was tested. Zebrafish larvae from the line Tg (fabp10a:DsRed) were incubated for 24 h with 1% and 2% ethanol (EtOH), 5 mg/mL of MI with 1% EtOH, and 5 mg/mL of MI with 2% EtOH. No significant differences between the groups with EtOH and the group treated with EtOH with MI were observed. Our results suggest that MI has no positive benefits on hepatocytes of zebrafish larvae. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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Review

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18 pages, 1828 KiB

Open AccessReview

Selenium Status in Patients with Chronic Liver Disease: A Systematic Review and Meta-Analysis

by Yaduan Lin, Fanchen He, Shaoyan Lian, Binbin Xie, Ting Liu, Jiang He and Chaoqun Liu

Nutrients 2022, 14(5), 952; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14050952 - 23 Feb 2022

Cited by 15 | Viewed by 3424

Abstract

Background: The potential role of selenium in preventing chronic liver diseases remains controversial. This meta-analysis aimed to summarize the available evidence from observational studies and intervention trials that had evaluated the associations between body selenium status and chronic liver diseases. Methods: We comprehensively searched MEDLINE, Embase, Web of Science, and Cochrane Library from inception to April 2021. The study protocol was registered at PROSPERO (CRD42020210144). Relative risks (RR) for the highest versus the lowest level of selenium and standard mean differences (SMD) with 95% confidence intervals (CI) were pooled using random-effects models. Heterogeneity and publication bias were evaluated using the I² statistic and Egger’s regression test, respectively. Results: There were 50 studies with 9875 cases and 12975 population controls in the final analysis. Patients with hepatitis (SMD = −1.78, 95% CI: −2.22 to −1.34), liver cirrhosis (SMD = −2.06, 95% CI: −2.48 to −1.63), and liver cancer (SMD = −2.71, 95% CI: −3.31 to −2.11) had significantly lower selenium levels than controls, whereas there was no significant difference in patients with fatty liver diseases (SMD = 1.06, 95% CI: −1.78 to 3.89). Moreover, the meta-analysis showed that a higher selenium level was significantly associated with a 41% decrease in the incidence of significant advanced chronic liver diseases (RR = 0.59, 95% CI: 0.49 to 0.72). Conclusion: Our meta-analysis suggested that both body selenium status and selenium intake were negatively associated with hepatitis, cirrhosis, and liver cancer. However, the associations for fatty liver diseases were conflicting and need to be established in prospective trials. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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10 pages, 1741 KiB

Open AccessReview

Euphausia pacifica (North Pacific Krill): Review of Chemical Features and Potential Benefits of 8-HEPE against Metabolic Syndrome, Dyslipidemia, NAFLD, and Atherosclerosis

by Nanae Ishida, Hidetoshi Yamada and Masamichi Hirose

Nutrients 2021, 13(11), 3765; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13113765 - 25 Oct 2021

Cited by 8 | Viewed by 3315

Abstract

Marine n-3 fatty acids are well known to have health benefits. Recently, krill oil, which contains phospholipids, has been in the spotlight as an n-3 PUFA-containing oil. Euphausia pacifica (E. pacifica), also called North Pacific krill, is a small, red crustacean similar to shrimp that flourishes in the North Pacific Ocean. E. pacifica oil contains 8-hydroxyeicosapentaenoic acid (8-HEPE) at a level more than 10 times higher than Euphausia superba oil. 8-HEPE can activate the transcription of peroxisome proliferator-activated receptor alpha (PPARα), PPARγ, and PPARδ to levels 10, 5, and 3 times greater than eicosapentaenoic acid, respectively. 8-HEPE has beneficial effects against metabolic syndrome (reduction in body weight gain, visceral fat area, amount of gonadal white adipose tissue, and gonadal adipocyte cell size), dyslipidemia (reduction in serum triacylglycerol and low-density lipoprotein cholesterol and induction of serum high-density lipoprotein cholesterol), atherosclerosis, and nonalcoholic fatty liver disease (reduction in triglyceride accumulation and hepatic steatosis in the liver) in mice. Further studies should focus on the beneficial effects of North Pacific krill oil products and 8-HEPE on human health. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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21 pages, 738 KiB

Open AccessReview

N-3 Polyunsaturated Fatty Acids and Their Lipid Mediators as A Potential Immune–Nutritional Intervention: A Molecular and Clinical View in Hepatic Disease and Other Non-Communicable Illnesses

by Francisca Herrera Vielma, Rodrigo Valenzuela, Luis A. Videla and Jessica Zúñiga-Hernández

Nutrients 2021, 13(10), 3384; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103384 - 26 Sep 2021

Cited by 9 | Viewed by 2807

Abstract

In recent years, the beneficial effect of n-3 polyunsaturated fatty acids (n-3 PUFAs) intake on human health has been widely accepted in the field of immunonutrition. Today, we find a diversity of supplements based on n-3 PUFAs and/or minerals, vitamins and other substances. The main objective of this review is to discuss the importance of n-3 PUFAs and their derivatives on immunity and inflammatory status related to liver disease and other non-communicable illnesses. Based on the burden of liver diseases in 2019, more than two million people die from liver pathologies per year worldwide, because it is the organ most exposed to agents such as viruses, toxins and medications. Consequently, research conducted on n-3 PUFAs for liver disease has been gaining prominence with encouraging results, given that these fatty acids have anti-inflammatory and cytoprotective effects. In addition, it has been described that n-3 PUFAs are converted into a novel species of lipid intermediaries, specialized pro-resolving mediators (SPMs). At specific levels, SPMs improve the termination of inflammation as well as the repairing and regeneration of tissues, but they are deregulated in liver disease. Since evidence is still insufficient to carry out pharmacological trials to benefit the resolution of acute inflammation in non-communicable diseases, there remains a call for continuing preclinical and clinical research to better understand SPM actions and outcomes. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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13 pages, 1854 KiB

Open AccessReview

CREBH Systemically Regulates Lipid Metabolism by Modulating and Integrating Cellular Functions

by Yoshimi Nakagawa, Masaya Araki, Song-iee Han, Yuhei Mizunoe and Hitoshi Shimano

Nutrients 2021, 13(9), 3204; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13093204 - 15 Sep 2021

Cited by 2 | Viewed by 3259

Abstract

Cyclic AMP-responsive element-binding protein H (CREBH, encoded by CREB3L3) is a membrane-bound transcriptional factor expressed in the liver and small intestine. The activity of CREBH is regulated not only at the transcriptional level but also at the posttranslational level. CREBH governs triglyceride metabolism in the liver by controlling gene expression, with effects including the oxidation of fatty acids, lipophagy, and the expression of apolipoproteins related to the lipoprotein lipase activation and suppression of lipogenesis. The activation and functions of CREBH are controlled in response to the circadian rhythm. On the other hand, intestinal CREBH downregulates the absorption of lipids from the diet. CREBH deficiency in mice leads to severe hypertriglyceridemia and fatty liver in the fasted state and while feeding a high-fat diet. Therefore, when crossing CREBH knockout (KO) mice with an atherosclerosis model, low-density lipoprotein receptor KO mice, these mice exhibit severe atherosclerosis. This phenotype is seen in both liver- and small intestine-specific CREBH KO mice, suggesting that CREBH controls lipid homeostasis in an enterohepatic interaction. This review highlights that CREBH has a crucial role in systemic lipid homeostasis to integrate cellular functions related to lipid metabolism. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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16 pages, 2535 KiB

Open AccessSystematic Review

Effect of Coffee Consumption on Non-Alcoholic Fatty Liver Disease Incidence, Prevalence and Risk of Significant Liver Fibrosis: Systematic Review with Meta-Analysis of Observational Studies

by Maryam Ebadi, Stephen Ip, Rahima A. Bhanji and Aldo J. Montano-Loza

Nutrients 2021, 13(9), 3042; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13093042 - 30 Aug 2021

Cited by 24 | Viewed by 6034

Abstract

Background and aim: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide. Given the anti-fibrotic and antioxidant properties of coffee, this systematic review and meta-analysis aims to provide updated results on the impact of coffee consumption on NAFLD incidence, prevalence, and risk of significant liver fibrosis. Methods: We conducted a comprehensive search in MEDLINE (OvidSP) and Scopus from January 2010 through January 2021. Relative risks for the highest versus the lowest level of coffee consumption were pooled using random-effects models. Heterogeneity and publication bias were evaluated using the Higgins’ I² statistic and Egger’s regression test, respectively. Results: Eleven articles consisting of two case-control studies, eight cross-sectional studies, and one prospective cohort study were included in the meta-analysis. Of those, three studies with 92,075 subjects were included in the analysis for NAFLD incidence, eight studies with 9558 subjects for NAFLD prevalence, and five with 4303 subjects were used for the analysis of liver fibrosis. There was no association between coffee consumption and NAFLD incidence (RR 0.88, 95% CI 0.63–1.25, p = 0.48) or NAFLD prevalence (RR 0.88, 95% CI 0.76–1.02, p = 0.09). The meta-analysis showed coffee consumption to be significantly associated with a 35% decreased odds of significant liver fibrosis (RR 0.65, 95% CI 0.54–0.78, p < 0.00001). There was no heterogeneity (I² = 11%, p = 0.34) and no evidence of publication bias (p = 0.134). Conclusion: This meta-analysis supports the protective role of coffee consumption on significant liver fibrosis in patients with NAFLD. However, the threshold of coffee consumption to achieve hepatoprotective effects needs to be established in prospective trials. Full article

(This article belongs to the Special Issue Nutrition and Liver Disease)

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