Pharmacotherapy of metabolically associated fatty liver disease

Metabolic dysfunction-associated fatty liver disease (MAFLD) is a progressive disease that is closely associated with metabolic disorders such as insulin resistance, obesity, dyslipidemia, and hypertension. In recent years, there has been an increase in the incidence of MAFLD, requiring the development of effective therapeutic approaches. Objective. To review the current pharmacological therapies of metabolic dysfunction-associated fatty liver disease and assess their effectiveness in the context of clinical trials. Materials and methods. The article reviews publications from 2019 to the present from the PubMed, Scopus, Web of Science, and eLibrary databases. Included are clinical studies, meta-analyses, and systematic reviews that assess therapeutic strategies to reduce steatosis, improve liver histological markers, and correct metabolic disorders. Results. The use of GLP-1 (glucagon-like peptide-1) receptor agonists improved the metabolic profile and histological parameters, including a reduction of inflammation and fibrosis. The ability of SGLT2 (Sodium-Glucose Co-Transporter 2) inhibitors to reduce blood glucose levels and improve liver function has been demonstrated and confirmed by visualization and biochemical indicators. Hepatoprotectors were moderately effective; however, their use in patients with disease progression was limited. The potential of agents activating peroxisome proliferator receptors in improving the histological and metabolic characteristics of the liver has been reported, which opens up new prospects in the treatment of MAFLD. Conclusion. The pharmacotherapy of metabolic dysfunction-associated fatty liver disease requires an integrated approach aimed at correcting underlying metabolic disorders. GLP-1 agonists and SGLT2 inhibitors significantly improve the metabolic profile and histological markers of the liver. Hepatoprotectors and antioxidants demonstrate moderate effectiveness. Promising results have been obtained for agents that activate peroxisome proliferator receptors; however, more studies are needed to assess their clinical significance.