Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Nonalcoholic Fatty Liver Disease/Metabolic Associated Fatty Liver Disease: New Insights...
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Nonalcoholic Fatty Liver Disease/Metabolic Associated Fatty Liver Disease: New Insights 3.0

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: 28 June 2024 | Viewed by 6175

Special Issue Editors

Dr. Andrea Dalbeni

E-Mail
Guest Editor
Hypertension and Liver Unit, Section of General Medicine, University of Verona, Verona, Italy
Interests: liver diseases; NAFLD; metabolic syndrome; cardiovascular complication in liver disease
Special Issues, Collections and Topics in MDPI journals
Dr. Alessandro Mantovani

E-Mail Website
Guest Editor
Section of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Verona, 37126 Verona, Italy
Interests: NAFLD; diabetes; ceramics; gender disparity in science
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nonalcoholic fatty liver disease (NAFLD) is an important health care problem worldwide. It affects 30% of adults in the general population, 70% of patients with type 2 diabetes (T2DM), and all patients with obesity. Importantly, NAFLD is now the second most frequent indication for liver transplantation in the United States. In the last several decades, it has become evident that NAFLD is not only associated with serious liver-related complications but also with relevant metabolic, cardiovascular, and renal complications. Although the pathogenesis of NAFLD is complex, it was established that NAFLD is strongly linked to insulin resistance, abdominal obesity, and T2DM. Based on this evidence, in 2020, some authors have proposed the change of the terminology from NAFLD to metabolic-associated fatty liver disease (MAFLD), as well as an update of the definition of this fatty liver disease. Regardless of the terminology used, however, it is clear that NAFLD/MAFLD is a dynamic disease, characterized by many factors that change over time. In this regard, specific phenotypes of NAFLD/MAFLD may be broadly driven by environmental factors, genetic predisposition, or metabolic factors.

This Special Issue of the International Journal of Molecular Sciences will focus on recent developments in the area of NAFLD/MAFLD pathogenesis and treatment, as well as new insights into the mechanisms and therapies for NAFLD/MAFLD. It will cover a selection of recent research topics and current review articles in the field of NAFLD/MAFLD. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Dr. Andrea Dalbeni
Dr. Alessandro Mantovani
Guest Editors

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 (NAFLD)
  • metabolic associated fatty liver disease (MAFLD)
  • nonalcoholic steatohepatitis (NASH)
  • fatty liver
  • cardiovascular disease

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review, Other

11 pages, 465 KiB  
Article
Glomerular Hyperfiltration: A Marker of Fibrosis Severity in Metabolic Associated Steatotic Liver Disease in an Adult Population
by Andrea Dalbeni, Marta Garbin, Mirko Zoncapè, Sara Romeo, Filippo Cattazzo, Anna Mantovani, Annalisa Cespiati, Anna Ludovica Fracanzani, Emmanouil Tsochatzis, David Sacerdoti, Alessandro Mantovani and Rosa Lombardi
Int. J. Mol. Sci. 2023, 24(21), 15837; https://doi.org/10.3390/ijms242115837 - 31 Oct 2023
Cited by 2 | Viewed by 1075
Abstract
Glomerular hyperfiltration (GH) is an increase in the glomerular filtration rate, possibly progressing to chronic kidney disease (CKD). Metabolic-associated steatotic liver disease (MASLD) is linked to an increased risk of CKD, especially if fibrosis is present; however, the association between GH and MASLD [...] Read more.
Glomerular hyperfiltration (GH) is an increase in the glomerular filtration rate, possibly progressing to chronic kidney disease (CKD). Metabolic-associated steatotic liver disease (MASLD) is linked to an increased risk of CKD, especially if fibrosis is present; however, the association between GH and MASLD has not been explored. To evaluate GH prevalence in MASLD and its possible correlation with liver fibrosis. 772 consecutive patients with ultrasound MASLD (mean age 47.3 ± 8.9 years, 67.1% males) were enrolled. GH was defined as estimated glomerular filtration rate (eGFR) greater than the upper quartile of values in the cohort. Liver stiffness measurement (LSM) by FibroScan ≥ 7.2 kPa suggested liver fibrosis. GH was present in 20% of patients, liver fibrosis in 30%. In total, 53.4% of the cohort was obese, 40.9% hypertensive, 36.3% diabetic and 70.8% dyslipidaemic. GH patients compared to non-GH were significantly younger (38.4 ± 8.3 vs. 49.5 ± 7.7, p < 0.001), with higher prevalence of LSM > 7.2 kPa (35.5% vs. 29%, p < 0.001), without any difference in metabolic comorbidities. In multivariate analysis, age (OR 0.85, CI 95% 0.82–0.87) and significant fibrosis (OR 1.83; CI 95%1.10–3.03) remained independently associated with GH, regardless of the presence of metabolic alterations and nephrotoxic drugs. GH, an early marker of renal damage, is highly prevalent in MASLD and is associated with hepatic fibrosis. GH may be considered an early marker of both liver and renal disease and its recognition could prompt the management of risk factors aimed at preventing the progression of both hepatic and renal disease. Full article
(This article belongs to the Special Issue Nonalcoholic Fatty Liver Disease/Metabolic Associated Fatty Liver Disease: New Insights 3.0)
►▼ Show Figures

Figure 1

Review

Jump to: Research, Other

34 pages, 3599 KiB  
Review
Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update
by Júlia Pauli De Cól, Enzo Pereira de Lima, Fernanda Moris Pompeu, Adriano Cressoni Araújo, Ricardo de Alvares Goulart, Marcelo Dib Bechara, Lucas Fornari Laurindo, Nahum Méndez-Sánchez and Sandra Maria Barbalho
Int. J. Mol. Sci. 2024, 25(7), 3694; https://doi.org/10.3390/ijms25073694 - 26 Mar 2024
Viewed by 741
Abstract
Metabolic-associated fatty liver disease (MAFLD) includes several metabolic dysfunctions caused by dysregulation in the brain–gut–liver axis and, consequently, increases cardiovascular risks and fatty liver dysfunction. In MAFLD, type 2 diabetes mellitus, obesity, and metabolic syndrome are frequently present; these conditions are related to [...] Read more.
Metabolic-associated fatty liver disease (MAFLD) includes several metabolic dysfunctions caused by dysregulation in the brain–gut–liver axis and, consequently, increases cardiovascular risks and fatty liver dysfunction. In MAFLD, type 2 diabetes mellitus, obesity, and metabolic syndrome are frequently present; these conditions are related to liver lipogenesis and systemic inflammation. This study aimed to review the connection between the brain–gut–liver axis and MAFLD. The inflammatory process, cellular alterations in hepatocytes and stellate cells, hypercaloric diet, and sedentarism aggravate the prognosis of patients with MAFLD. Thus, to understand the modulation of the physiopathology of MAFLD, it is necessary to include the organokines involved in this process (adipokines, myokines, osteokines, and hepatokines) and their clinical relevance to project future perspectives of this condition and bring to light new possibilities in therapeutic approaches. Adipokines are responsible for the activation of distinct cellular signaling in different tissues, such as insulin and pro-inflammatory cytokines, which is important for balancing substances to avoid MAFLD and its progression. Myokines improve the quantity and quality of adipose tissues, contributing to avoiding the development of MAFLD. Finally, hepatokines are decisive in improving or not improving the progression of this disease through the regulation of pro-inflammatory and anti-inflammatory organokines. Full article
(This article belongs to the Special Issue Nonalcoholic Fatty Liver Disease/Metabolic Associated Fatty Liver Disease: New Insights 3.0)
►▼ Show Figures

Figure 1

37 pages, 919 KiB  
Review
Osteosarcopenia in NAFLD/MAFLD: An Underappreciated Clinical Problem in Chronic Liver Disease
by Alessandra Musio, Federica Perazza, Laura Leoni, Bernardo Stefanini, Elton Dajti, Renata Menozzi, Maria Letizia Petroni, Antonio Colecchia and Federico Ravaioli
Int. J. Mol. Sci. 2023, 24(8), 7517; https://doi.org/10.3390/ijms24087517 - 19 Apr 2023
Cited by 3 | Viewed by 2848
Abstract
Chronic liver disease (CLD), including non-alcoholic fatty liver disease (NAFLD) and its advanced form, non-alcoholic steatohepatitis (NASH), affects a significant portion of the population worldwide. NAFLD is characterised by fat accumulation in the liver, while NASH is associated with inflammation and liver damage. [...] Read more.
Chronic liver disease (CLD), including non-alcoholic fatty liver disease (NAFLD) and its advanced form, non-alcoholic steatohepatitis (NASH), affects a significant portion of the population worldwide. NAFLD is characterised by fat accumulation in the liver, while NASH is associated with inflammation and liver damage. Osteosarcopenia, which combines muscle and bone mass loss, is an emerging clinical problem in chronic liver disease that is often underappreciated. The reductions in muscle and bone mass share several common pathophysiological pathways; insulin resistance and chronic systemic inflammation are the most crucial predisposing factors and are related to the presence and gravity of NAFLD and to the worsening of the outcome of liver disease. This article explores the relationship between osteosarcopenia and NAFLD/MAFLD, focusing on the diagnosis, prevention and treatment of this condition in patients with CLD. Full article
(This article belongs to the Special Issue Nonalcoholic Fatty Liver Disease/Metabolic Associated Fatty Liver Disease: New Insights 3.0)
►▼ Show Figures

Figure 1

Other

Jump to: Research, Review

8 pages, 634 KiB  
Brief Report
PNPLA3 rs738409 Genetic Variant Inversely Correlates with Platelet Count, Thereby Affecting the Performance of Noninvasive Scores of Hepatic Fibrosis
by Marica Meroni and Paola Dongiovanni
Int. J. Mol. Sci. 2023, 24(20), 15046; https://doi.org/10.3390/ijms242015046 - 10 Oct 2023
Cited by 1 | Viewed by 913
Abstract
Noninvasive tests (NITs) including platelets (PLTs) have been proposed to replace hepatic biopsy for the diagnosis of nonalcoholic fatty liver disease (NAFLD), or as more recently redefined, metabolic dysfunction-associated steatotic liver disease (MASLD). There has been reported an inverse correlation between PLTs and [...] Read more.
Noninvasive tests (NITs) including platelets (PLTs) have been proposed to replace hepatic biopsy for the diagnosis of nonalcoholic fatty liver disease (NAFLD), or as more recently redefined, metabolic dysfunction-associated steatotic liver disease (MASLD). There has been reported an inverse correlation between PLTs and progressive MASLD, which is also affected by the patatin-like phospholipase domain-containing protein 3 (PNPLA3) rs738409 C>G mutation. However, the correlation between low PLTs and PNPLA3 genotype has been poorly investigated. We stratified 1155 biopsy-proven MASLD patients according to PNPLA3 genotype. The hepatic expression of genes involved in megakaryopoiesis was investigated in n = 167 bariatric patients by RNAseq. PLT count progressively decreased according to the number of PNPLA3 at-risk alleles, irrespective of the presence of advanced fibrosis. The hepatic expression of genes involved in PLT biogenesis was associated with the PNPLA3 GG genotype. Finally, the presence of the PNPLA3 homozygosity flattened the accuracy of fibrosis-4 (FIB-4) in discriminating histological fibrosis stages. The PNPLA3 GG genotype may underpower the accuracy of NITs which include PLT count in identifying those patients with potentially reversible stages of fibrosis. Full article
(This article belongs to the Special Issue Nonalcoholic Fatty Liver Disease/Metabolic Associated Fatty Liver Disease: New Insights 3.0)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop