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Metabolic Associated Fatty Liver Disease: A New Definition

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 23490

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Special Issue Editor

Dr. Yoshio Sumida

E-Mail Website1 Website2
Guest Editor

1. Department of Hepatology and Pancreatology, Aichi Medical University of Medicine, Nagakute, Aichi, Japan;
2. Japan Strategic Medical Administration Research Center (J-SMARC), Nagoya, Aichi, Japan
Interests: Interests: nonalcoholic steatohepatitis; oxidative stress; hepatic fibrosis; diabetes mellitus; liver cirrhosis; hepatocellular carcinoma

Special Issue Information

Dear Colleagues,

Worldwide, 25% of the adult population suffers from nonalcoholic fatty liver disease (NAFLD). Until now, the exclusion of other chronic liver diseases including "excess" alcohol intake has been necessary to establish a diagnosis of NAFLD. Recently, a consensus of international experts proposed that the disease acronym be changed from NAFLD to metabolic (dysfunction)-associated fatty liver disease (MAFLD). The diagnostic criteria of MAFLD are based on evidence of hepatic steatosis, in addition to one of the following three criteria, namely overweight/obesity, presence of type 2 diabetes, or evidence of metabolic dysregulation. MAFLD is a novel concept proposed in 2020, the utility of which has not been tested and validated in the real world. MAFLD can coexist with other liver diseases. Therefore, MAFLD plus a hepatitis B virus (HBV) inactive carrier, MAFLD plus alcoholic liver disease (ALD), MAFLD plus autoimmune hepatitis (AIH), or MAFLD plus drug-induced liver injury (DILI) are plausible as a final diagnosis in clinical practice. MAFLD definition is more practical for identifying patients with fatty liver disease with a high risk of disease progression. This Special Issue will include papers investigating the pathological mechanisms, diagnostics using new biomarkers, and treatment strategies in MAFLD. Furthermore, experimental in vitro and in vivo studies examining potential new approaches to attenuate MAFLD are welcome. This Special Issue welcomes original research and review papers regarding MAFLD.

Dr. Yoshio Sumida
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

• Nonalcoholic fatty liver disease
• Metabolism-associated fatty liver disease
• Hepatocellular carcinoma
• Type 2 diabetes
• Hepatic fibrosis
• Liver cirrhosis
• PNPLA3
• Obesity
• Metabolic syndrome

Published Papers (3 papers)

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Research

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22 pages, 5127 KiB

Open AccessArticle

The Ameliorative Effects of Saikosaponin in Thioacetamide-Induced Liver Injury and Non-Alcoholic Fatty Liver Disease in Mice

by Geng-Ruei Chang, Wei-Li Lin, Tzu-Chun Lin, Huei-Jyuan Liao and Yu-Wen Lu

Int. J. Mol. Sci. 2021, 22(21), 11383; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111383 - 21 Oct 2021

Cited by 31 | Viewed by 3343

Abstract

Liver disorders are a major health concern. Saikosaponin-d (SSd) is an effective active ingredient extracted from Bupleurum falcatum, a traditional Chinese medicinal plant, with anti-inflammatory and antioxidant properties. However, its hepatoprotective properties and underlying mechanisms are unknown. We investigated the effects and underlying mechanisms of SSd treatment for thioacetamide (TAA)-induced liver injury and high-fat-diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) in male C57BL/6 mice. The SSd group showed significantly higher food intake, body weight, and hepatic antioxidative enzymes (catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD)) and lower hepatic cyclooxygenase-2 (COX-2), serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and fibroblast growth factor-21 (FGF21) compared with controls, as well as reduced expression of inflammation-related genes (nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS)) messenger RNA (mRNA). In NAFLD mice, SSd reduced serum ALT, AST, triglycerides, fatty acid–binding protein 4 (FABP4) and sterol regulatory element–binding protein 1 (SREBP1) mRNA, and endoplasmic reticulum (ER)-stress-related proteins (phosphorylated eukaryotic initiation factor 2α subunit (p-eIF2α), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP). SSd has a hepatoprotective effect in liver injury by suppressing inflammatory responses and acting as an antioxidant. Full article

(This article belongs to the Special Issue Metabolic Associated Fatty Liver Disease: A New Definition)

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Review

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23 pages, 3090 KiB

Open AccessReview

Xenobiotic-Induced Aggravation of Metabolic-Associated Fatty Liver Disease

by Julie Massart, Karima Begriche, Anne Corlu and Bernard Fromenty

Int. J. Mol. Sci. 2022, 23(3), 1062; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031062 - 19 Jan 2022

Cited by 19 | Viewed by 3198

Abstract

Metabolic-associated fatty liver disease (MAFLD), which is often linked to obesity, encompasses a large spectrum of hepatic lesions, including simple fatty liver, steatohepatitis, cirrhosis and hepatocellular carcinoma. Besides nutritional and genetic factors, different xenobiotics such as pharmaceuticals and environmental toxicants are suspected to aggravate MAFLD in obese individuals. More specifically, pre-existing fatty liver or steatohepatitis may worsen, or fatty liver may progress faster to steatohepatitis in treated patients, or exposed individuals. The mechanisms whereby xenobiotics can aggravate MAFLD are still poorly understood and are currently under deep investigations. Nevertheless, previous studies pointed to the role of different metabolic pathways and cellular events such as activation of de novo lipogenesis and mitochondrial dysfunction, mostly associated with reactive oxygen species overproduction. This review presents the available data gathered with some prototypic compounds with a focus on corticosteroids and rosiglitazone for pharmaceuticals as well as bisphenol A and perfluorooctanoic acid for endocrine disruptors. Although not typically considered as a xenobiotic, ethanol is also discussed because its abuse has dire consequences on obese liver. Full article

(This article belongs to the Special Issue Metabolic Associated Fatty Liver Disease: A New Definition)

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26 pages, 1363 KiB

Open AccessReview

Role of Insulin Resistance in MAFLD

by Yoshitaka Sakurai, Naoto Kubota, Toshimasa Yamauchi and Takashi Kadowaki

Int. J. Mol. Sci. 2021, 22(8), 4156; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084156 - 16 Apr 2021

Cited by 127 | Viewed by 15980

Abstract

Many studies have reported that metabolic dysfunction is closely involved in the complex mechanism underlying the development of non-alcoholic fatty liver disease (NAFLD), which has prompted a movement to consider renaming NAFLD as metabolic dysfunction-associated fatty liver disease (MAFLD). Metabolic dysfunction in this context encompasses obesity, type 2 diabetes mellitus, hypertension, dyslipidemia, and metabolic syndrome, with insulin resistance as the common underlying pathophysiology. Imbalance between energy intake and expenditure results in insulin resistance in various tissues and alteration of the gut microbiota, resulting in fat accumulation in the liver. The role of genetics has also been revealed in hepatic fat accumulation and fibrosis. In the process of fat accumulation in the liver, intracellular damage as well as hepatic insulin resistance further potentiates inflammation, fibrosis, and carcinogenesis. Increased lipogenic substrate supply from other tissues, hepatic zonation of Irs1, and other factors, including ER stress, play crucial roles in increased hepatic de novo lipogenesis in MAFLD with hepatic insulin resistance. Herein, we provide an overview of the factors contributing to and the role of systemic and local insulin resistance in the development and progression of MAFLD. Full article

(This article belongs to the Special Issue Metabolic Associated Fatty Liver Disease: A New Definition)

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