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Cited by 81Liver Disease Diagnosis and TreatmentLiver physiology and pathologyDiet, Metabolism, and Disease

A Comparison of the Gene Expression Profiles of Non-Alcoholic Fatty Liver Disease between Animal Models of a High-Fat Diet and Methionine-Choline-Deficient Diet

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Alshawsh, Mohammed Abdullah, Alsalahi, Abdulsamad, Alshehade, Salah Abdalrazak, Saghir, Sultan Ayesh Mohammed, Ahmeda, Ahmad Faheem, Al Zarzour, Raghdaa Hamdan, Mahmoud, Ayman Moawad·2022·Molecules
DOI 10.3390/molecules27030858PMC PMC8839835
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Abstract

Non-alcoholic fatty liver disease (NAFLD) embraces several forms of liver disorders involving fat disposition in hepatocytes ranging from simple steatosis to the severe stage, namely, non-alcoholic steatohepatitis (NASH). Recently, several experimental in vivo animal models for NAFLD/NASH have been established. However, no reproducible experimental animal model displays the full spectrum of pathophysiological, histological, molecular, and clinical features associated with human NAFLD/NASH progression. Although methionine-choline-deficient (MCD) diet and high-fat diet (HFD) models can mimic histological and metabolic abnormalities of human disease, respectively, the molecular signaling pathways are extremely important for understanding the pathogenesis of the disease. This review aimed to assess the differences in gene expression patterns and NAFLD/NASH progression pathways among the most common dietary animal models, i.e., HFD- and MCD diet-fed animals. Studies showed that the HFD and MCD diet could induce either up- or downregulation of the expression of genes and proteins that are involved in lipid metabolism, inflammation, oxidative stress, and fibrogenesis pathways. Interestingly, the MCD diet model could spontaneously develop liver fibrosis within two to four weeks and has significant effects on the expression of genes that encode proteins and enzymes involved in the liver fibrogenesis pathway. However, such effects in the HFD model were found to occur after 24 weeks with insulin resistance but appear to cause less severe fibrosis. In conclusion, assessing the abnormal gene expression patterns caused by different diet types provides valuable information regarding the molecular mechanisms of NAFLD/NASH and predicts the clinical progression of the disease. However, expression profiling studies concerning genetic variants involved in the development and progression of NAFLD/NASH should be conducted.

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Authors
Alshawsh, M. A., Alsalahi, A., Alshehade, S. A., Saghir, S. A. M., Ahmeda, A. F., Al Zarzour, R. H., & Mahmoud, A. M.
Affiliations
  • University of Malaya (MY)
  • Universiti Sains Malaysia (MY)
  • Al-Hussein Bin Talal University (JO)
  • Ajman University (AE)
  • Discipline of Pharmacology, School of Pharmaceutical Sciences, Universiti Sains Malaysia (USM), Gelugor 11800, Malaysia
  • Beni-Suef University (EG)
Corresponding author
Alshawsh, Mohammed Abdullah
ORCID
Venue
Molecules
Publisher
MDPI AG
Published
2022-01-27
Volume
27
Issue
3
Pages
858
ISSN
1420-3049 (ISSN-L)
DOI
10.3390/molecules27030858
PMC
PMC8839835
OpenAlex
W4210810023
Cited by
81
References
4
Citations by year
2026: 12 · 2025: 16 · 2024: 31 · 2023: 14 · 2022: 8
FWCI
12.45
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecules (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • e-space (Manchester Metropolitan University) (acceptedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
University of Malaya (ST070-2021)
Topics
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords
non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, animal models, high-fat diet, methionine-choline-deficient diet, gene expression profiling, liver fibrosis, lipid metabolism, inflammation, oxidative stress, insulin resistance, disease progression
MeSH terms
Animals, Choline, Choline Deficiency, Disease Models, Animal, Humans, Methionine, Hepatocytes, Mice, Diet, High-Fat, Transcriptome, Non-alcoholic Fatty Liver Disease

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