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Molecular Mechanisms of Fatty Liver and Metabolic/Malignant Events
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Molecular Mechanisms of Fatty Liver and Metabolic/Malignant Events

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

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 2979

Special Issue Editor

Prof. Dr. Takumi Kawaguchi

E-Mail Website
Guest Editor
Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, Kurume 830-0011, Japan
Interests: nonalcoholic fatty liver disease; metabolic dysfunction-associated fatty liver disease; insulin resistance; hepatic fibrosis; hepatocellular carcinoma; extrahepatic malignancies; exercise therapy; nutritional therapy; bariatric surgery

Special Issue Information

Dear Colleagues,

A Special Issue on the hot topic "Molecular Mechanisms of Fatty Liver and Metabolic/Malignant Events" is being prepared for the journal IJMS. Fatty liver is a common disease worldwide. Since the liver plays a crucial role in the homeostasis of various metabolic pathways, fatty liver may be a risk factor for a variety of metabolic dysfunctions including diabetes mellitus and hyperlipidemia. In addition, fatty liver is a major cause of hepatocellular carcinoma. Moreover, fatty liver is known as a risk for extrahepatic malignancies. Thus, fatty liver may promote the onset of metabolic and malignant events. However, limited information is available for molecular and clinical mechanisms for metabolic/malignant events caused by fatty liver. Furthermore, it remains unclear if therapeutic intervention for fatty liver affects metabolic/malignant events.

In this Research Topic, we invite expert scholars in this area to contribute both original research and review articles that elucidate novel aspects of the main molecular and cellular signaling pathways involved in the metabolic and malignant events related with fatty liver. Prospective topics include but are not limited to the role of lipids accumulation, insulin resistance, oxidative damage, and fibrosis response in cellular mechanisms, alterations in lipid metabolism enzymes, epigenetics involved in fatty liver and metabolism, and relevant molecular experimental models.

Prof. Dr. Takumi Kawaguchi
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
  • metabolic-dysfunction-associated fatty liver disease
  • hepatocellular carcinoma
  • extrahepatic malignancies
  • atherosclerotic cardiovascular disease
  • sleep apnea syndrome
  • chronic obstructive pulmonary disease

Published Papers (1 paper)

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Research

17 pages, 59158 KiB  
Article
Proglumide Reverses Nonalcoholic Steatohepatitis by Interaction with the Farnesoid X Receptor and Altering the Microbiome
by Martha D. Gay, Hong Cao, Narayan Shivapurkar, Sivanesan Dakshanamurthy, Bhaskar Kallakury, Robin D. Tucker, John Kwagyan and Jill P. Smith
Int. J. Mol. Sci. 2022, 23(3), 1899; https://doi.org/10.3390/ijms23031899 - 8 Feb 2022
Cited by 5 | Viewed by 2555
Abstract
Nonalcoholic steatohepatitis (NASH) is associated with obesity, metabolic syndrome, and dysbiosis of the gut microbiome. Cholecystokinin (CCK) is released by saturated fats and plays an important role in bile acid secretion. CCK receptors are expressed on cholangiocytes, and CCK-B receptor expression increases in [...] Read more.
Nonalcoholic steatohepatitis (NASH) is associated with obesity, metabolic syndrome, and dysbiosis of the gut microbiome. Cholecystokinin (CCK) is released by saturated fats and plays an important role in bile acid secretion. CCK receptors are expressed on cholangiocytes, and CCK-B receptor expression increases in the livers of mice with NASH. The farnesoid X receptor (FXR) is involved in bile acid transport and is a target for novel therapeutics for NASH. The aim of this study was to examine the role of proglumide, a CCK receptor inhibitor, in a murine model of NASH and its interaction at FXR. Mice were fed a choline deficient ethionine (CDE) diet to induce NASH. Some CDE-fed mice received proglumide-treated drinking water. Blood was collected and liver tissues were examined histologically. Proglumide’s interaction at FXR was evaluated by computer modeling, a luciferase reporter assay, and tissue FXR expression. Stool microbiome was analyzed by RNA-Sequencing. CDE-fed mice developed NASH and the effect was prevented by proglumide. Computer modeling demonstrated specific binding of proglumide to FXR. Proglumide binding in the reporter assay was consistent with a partial agonist at the FXR with a mean binding affinity of 215 nM. FXR expression was significantly decreased in livers of CDE-fed mice compared to control livers, and proglumide restored FXR expression to normal levels. Proglumide therapy altered the microbiome signature by increasing beneficial and decreasing harmful bacteria. These data highlight the potential novel mechanisms by which proglumide therapy may improve NASH through interaction with the FXR and consequent alteration of the gut microbiome. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Fatty Liver and Metabolic/Malignant Events)
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