Metabolically associated fatty liver disease – a disease of the 21st century: A review
- Authors: Maev I.V.1, Andreev D.N.1, Kucheryavyy Y.A.2
-
Affiliations:
- Yevdokimov Moscow State University of Medicine and Dentistry
- Ilyinskaya Hospital
- Issue: Vol 24, No 5 (2022)
- Pages: 325-332
- Section: Gastroenterology
- URL: https://ogarev-online.ru/2075-1753/article/view/112444
- DOI: https://doi.org/10.26442/20751753.2022.5.201532
- ID: 112444
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Abstract
Metabolically associated fatty liver disease (MAFLD) is a widespread chronic disease characterized by increased accumulation of fat in the liver, which is based on metabolic dysfunction. The incidence of MAFLD is well over 20% in most regions of the world and is on an increasing trend. Current thinking considers the etiology and pathogenesis of MAFLD under the concept of "multiple parallel blows". According to this model, the development and progression of the disease are due to the interaction of multiple genetic, environmental and adaptive factors, which include specific genetic polymorphisms (e.g., the PNPLA3 gene) and epigenetic modifications, dietary patterns (e.g. high saturated fat and fructose intake), sedentary activity, obesity, insulin resistance, dysregulation of adipokines, lipotoxicity, oxidative stress, and gut microbiota dysbiosis (small intestinal bacterial overgrowth syndrome). The basis for the diagnosis of MAFLD is the presence of proven hepatic steatosis in combination with one of the following criteria: overweight/obesity, presence of type 2 diabetes mellitus, signs of metabolic dysregulation. Nonmedicamental therapies recommended for patients with MAFLD include weight loss (if overweight or obese), reduction of saturated fatty acid and fructose intake, and inclusion of adequate amounts of omega-3 polyunsaturated fatty acids and dietary fibre (psyllium) in the diet. Pharmacotherapy of MAFLD should be aimed at correcting insulin resistance, improving liver function and reducing the risk of associated diseases.
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##article.viewOnOriginalSite##About the authors
Igor V. Maev
Yevdokimov Moscow State University of Medicine and Dentistry
Email: dna-mit8@mail.ru
ORCID iD: 0000-0001-6114-564X
D. Sci. (Med.), Prof., Acad. RAS, Yevdokimov Moscow State University of Medicine and Dentistry
Russian Federation, MoscowDmitry N. Andreev
Yevdokimov Moscow State University of Medicine and Dentistry
Author for correspondence.
Email: dna-mit8@mail.ru
ORCID iD: 0000-0002-4007-7112
Cand. Sci. (Med.), Yevdokimov Moscow State University of Medicine and Dentistry
Russian Federation, MoscowYury A. Kucheryavyy
Ilyinskaya Hospital
Email: proped@mail.ru
ORCID iD: 0000-0001-7760-2091
Cand. Sci. (Med.), Ilyinskaya Hospital
Russian Federation, Glukhovo, Moscow RegionReferences
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