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Biomolecules
Special Issues
Molecular Pathology and Therapeutics in Non-alcoholic Fatty Liver Disease
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Molecular Pathology and Therapeutics in Non-alcoholic Fatty Liver Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: closed (31 May 2020) | Viewed by 19864

Special Issue Editor

Prof. Dr. Naoki Tanaka

E-Mail Website
Guest Editor
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
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The worldwide spread of a sedentary lifestyle and excess food consumption has increased the prevalence of non-alcoholic fatty liver disease (NAFLD) in many countries among a larger number of generations. NAFLD is closely associated with obesity, insulin resistance, dyslipidemia, atherosclerosis, and systemic inflammation, which represent hepatic manifestations of metabolic syndrome. NAFLD is not only a risk factor for the occurrence of diabetes and cardiovascular events, but also may progress to non-alcoholic steatohepatitis (NASH), hepatic fibrosis, and hepatocellular carcinoma, eventually leading to death. NAFLD/NASH is, therefore, considered to be a detrimental condition necessitating appropriate therapeutic interventions. To date, however, the establishment of effective therapeutics has been challenging, likely due to the multiple factors that are involved in NAFLD/NASH pathogenesis, including complex nutrient metabolism, microbiome–gut metabolite interaction, and inter-organ networks. In this Special Issue, we would like to review our current understanding of the pathogenesis of and therapies for NAFLD/NASH and discuss future directions for research on NAFLD/NASH.

Dr. Naoki Tanaka
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • glucose, fat, and amino acid metabolism
  • micronutrients and food contaminants
  • inflammation, oxidative stress, and ER stress
  • autophagy and apoptosis
  • Insulin and G-protein-coupled receptor signaling
  • microbiome and gut metabolites
  • crosstalk between the liver and extrahepatic organs, such as brain, muscle, and adipose tissue
  • diet composition
  • non-alcoholic fatty liver disease (NAFLD) and hepatic fibrosis
  • NAFLD and hepatocarcinogenesis

Published Papers (2 papers)

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Review

64 pages, 4254 KiB  
Review
Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants
by Clémence Rives, Anne Fougerat, Sandrine Ellero-Simatos, Nicolas Loiseau, Hervé Guillou, Laurence Gamet-Payrastre and Walter Wahli
Biomolecules 2020, 10(12), 1702; https://doi.org/10.3390/biom10121702 - 21 Dec 2020
Cited by 80 | Viewed by 11185
Abstract
Non-alcoholic fatty liver disease (NAFLD) is often the hepatic expression of metabolic syndrome and its comorbidities that comprise, among others, obesity and insulin-resistance. NAFLD involves a large spectrum of clinical conditions. These range from steatosis, a benign liver disorder characterized by the accumulation [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is often the hepatic expression of metabolic syndrome and its comorbidities that comprise, among others, obesity and insulin-resistance. NAFLD involves a large spectrum of clinical conditions. These range from steatosis, a benign liver disorder characterized by the accumulation of fat in hepatocytes, to non-alcoholic steatohepatitis (NASH), which is characterized by inflammation, hepatocyte damage, and liver fibrosis. NASH can further progress to cirrhosis and hepatocellular carcinoma. The etiology of NAFLD involves both genetic and environmental factors, including an unhealthy lifestyle. Of note, unhealthy eating is clearly associated with NAFLD development and progression to NASH. Both macronutrients (sugars, lipids, proteins) and micronutrients (vitamins, phytoingredients, antioxidants) affect NAFLD pathogenesis. Furthermore, some evidence indicates disruption of metabolic homeostasis by food contaminants, some of which are risk factor candidates in NAFLD. At the molecular level, several models have been proposed for the pathogenesis of NAFLD. Most importantly, oxidative stress and mitochondrial damage have been reported to be causative in NAFLD initiation and progression. The aim of this review is to provide an overview of the contribution of nutrients and food contaminants, especially pesticides, to oxidative stress and how they may influence NAFLD pathogenesis. Full article
(This article belongs to the Special Issue Molecular Pathology and Therapeutics in Non-alcoholic Fatty Liver Disease)
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16 pages, 817 KiB  
Review
Metabolic Functions of G Protein-Coupled Receptors in Hepatocytes—Potential Applications for Diabetes and NAFLD
by Takefumi Kimura, Sai P. Pydi, Jonathan Pham and Naoki Tanaka
Biomolecules 2020, 10(10), 1445; https://doi.org/10.3390/biom10101445 - 15 Oct 2020
Cited by 22 | Viewed by 8268
Abstract
G protein-coupled receptors (GPCRs) are cell surface receptors that mediate the function of extracellular ligands. Understanding how GPCRs work at the molecular level has important therapeutic implications, as 30–40% of the drugs currently in clinical use mediate therapeutic effects by acting on GPCRs. [...] Read more.
G protein-coupled receptors (GPCRs) are cell surface receptors that mediate the function of extracellular ligands. Understanding how GPCRs work at the molecular level has important therapeutic implications, as 30–40% of the drugs currently in clinical use mediate therapeutic effects by acting on GPCRs. Like many other cell types, liver function is regulated by GPCRs. More than 50 different GPCRs are predicted to be expressed in the mouse liver. However, knowledge of how GPCRs regulate liver metabolism is limited. A better understanding of the metabolic role of GPCRs in hepatocytes, the dominant constituent cells of the liver, could lead to the development of novel drugs that are clinically useful for the treatment of various metabolic diseases, including type 2 diabetes, nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). In this review, we describe the functions of multiple GPCRs expressed in hepatocytes and their role in metabolic processes. Full article
(This article belongs to the Special Issue Molecular Pathology and Therapeutics in Non-alcoholic Fatty Liver Disease)
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