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Life
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Alcohol and Food Misuse Lead to Fatty Liver Diseases
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Alcohol and Food Misuse Lead to Fatty Liver Diseases

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 3065

Special Issue Editors

Dr. Stephen D. H. Malnick

E-Mail Website
Guest Editor
Department of Internal Medicine C, Kaplan Medical Center, Rehovot 76100, Israel
Interests: alcoholic liver disease; non-alcoholic liver disease; intestinal microbiome; hepatitis C; COVID-19
Dr. Manuela G. Neuman

E-Mail Website
Guest Editor
In Vitro Drug Safety and Biotechnology and Department of Pharmacology and Toxicology, Faculty of Medicine, Banting Institute, University of Toronto, 100 College Street, Toronto, ON M5G 1L5, Canada
Interests: alcoholic liver disease; non-alcoholic steatohepatitis; hepatocytotoxicity; inflammatory biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The liver has a unique blood supply from both portal and systemic sources. Portal blood is delivered to the liver directly via absorption from the GI tract. This includes both substances that are ingested and also substances that are either produced or metabolized by the intestinal microbiome.

Hepatic steatosis is a result of either alcohol ingestion or changes in hepatic metabolism linked to metabolic syndrome, including endogenous alcohol production. Steatosis may progress via steatohepatitis, fibrosis and cirrhosis and its complication include hepatocellular carcinoma.

As a result of the worldwide epidemic of obesity, metabolic-associated fatty liver disease (MAFLD) is very common with a prevalence of more than 30% in developed countries. Alcohol use has also increased, linked to the COVID-19 pandemic. The combination of these 2 drivers has had a major effect on alcoholic and metabolic-associated fatty liver disease.

It is the aim of this special edition to review the pathogenesis of hepatic steatosis, the clinical features, diagnosis and management of these two disorders. We will explore both the common mechanistic systems and the involvement of the microbiome.

Dr. Stephen D.H. Malnick
Prof. Dr. Neuman Manuela
Guest Editors

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Keywords

  • metabolic associated fatty liver disease - MAFLD
  • alcoholic liver disease
  • non-alcoholic steatohepatitis
  • alcohol and COVID
  • cytokine storm
  • microbiome

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Published Papers (1 paper)

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Research

12 pages, 1379 KiB  
Article
Effectiveness of One-Year Pemafibrate Therapy on Non-Alcoholic Fatty Liver Disease Refractory to Long-Term Sodium Glucose Cotransporter-2 Inhibitor Therapy: A Pilot Study
by Satoshi Shinozaki, Toshiyuki Tahara, Kouichi Miura, Alan Kawarai Lefor and Hironori Yamamoto
Life 2023, 13(6), 1327; https://doi.org/10.3390/life13061327 - 5 Jun 2023
Cited by 2 | Viewed by 2712
Abstract
Background: Both pemafibrate and sodium glucose cotransporter-2 (SGLT2) inhibitor can decrease serum transaminase levels in patients with non-alcoholic fatty liver disease (NAFLD) complicated with dyslipidemia and type 2 diabetes mellitus (T2DM), respectively. However, the effectiveness of combined therapy has been rarely reported. Methods: [...] Read more.
Background: Both pemafibrate and sodium glucose cotransporter-2 (SGLT2) inhibitor can decrease serum transaminase levels in patients with non-alcoholic fatty liver disease (NAFLD) complicated with dyslipidemia and type 2 diabetes mellitus (T2DM), respectively. However, the effectiveness of combined therapy has been rarely reported. Methods: This is a two-center retrospective observational study. NAFLD patients complicated with T2DM treated with pemafibrate for >1 year were included, in whom prior treatment with SGLT2 inhibitor > 1 year failed to normalize serum alanine aminotransferase (ALT) levels. Hepatic inflammation, function, and fibrosis were assessed by ALT, albumin-bilirubin (ALBI) score, and Mac-2 binding protein glycosylation isomer (M2BPGi) levels, respectively. Results: Seven patients were included. The median duration of prior treatment with SGLT2 inhibitors was 2.3 years. During the one year before starting pemafibrate therapy, the therapy did not significantly change hepatic enzymes. All patients received pemafibrate 0.1 mg twice daily without dose escalations. During one year of pemafibrate therapy, triglyceride, aspartate aminotransferase, ALT, γ-glutamyl transpeptidase, ALBI score, and M2BPGi levels significantly improved (p < 0.05), although weight or hemoglobin A1c did not significantly change. Conclusions: One year of pemafibrate therapy improves markers of hepatic inflammation, function, and fibrosis in NAFLD patients in whom long-term SGLT2 inhibitor therapy failed to normalize serum ALT. Full article
(This article belongs to the Special Issue Alcohol and Food Misuse Lead to Fatty Liver Diseases)
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