Abstract
Introduction. The pathogenesis of non-alcoholic fatty liver disease (NAFLD) is based on lipid accumulation in hepatocytes accompanied by oxidative stress and the development of steatohepatitis, whereas the etiology of alcoholic liver disease (ALD) is associated with acetaldehyde-induced cellular injury. Previous studies have demonstrated that in rats subjected to chronic alcoholization under immobilization stress, the metabolism of fucoglycoproteins (FGP) in the tissues of the liver, stomach, and small intestine shifts toward catabolism. In addition, experimental data indicate that prolonged feeding of animals with a fructose-rich diet combined with administration of S-adenosylmethionine (SAMe) leads to normalization of the metabolism of fucose-containing biopolymers.
The aim of the present study was to analyze changes in FGP metabolism in the liver, stomach, and small intestine of immobilized rats with NAFLD and ALD under conditions of SAMe administration.
Material and methods. The experiments were conducted on 64 adult male outbred white rats weighing 220 – 260 g. The animals were divided into two groups: in the first group, NAFLD was modeled using a high-fructose diet; in the second group, an ALD model was induced by intragastric administration of ethanol. Immobilization stress was applied to all animals by two-hour dorsal fixation. In addition, starting from day 21 of the experiment, rats in both groups received intramuscular injections of S-adenosylmethionine. To achieve the study objectives, histological examination of liver specimens and biochemical analyses (lipid profile, glucose concentration, corticosterone, insulin, and C-peptide levels) were performed on days 21, 35, 60, and 90 of the observation period.
Results. On days 21 and 35 of the NAFLD model, the formation of hepatic steatosis and inflammatory infiltration was observed. In contrast, in the ALD model, pathological changes became evident on day 60, which may be associated with ethanol metabolites that enhance oxidative stress.
Conclusion. The obtained data indicate that SAMe is capable of partially attenuating metabolic disturbances in fatty liver disease under conditions of chronic stress; however, it does not completely eliminate the catabolic alterations in fucoglycoprotein metabolism in the studied tissues.
Authors and affiliations
https://elibrary.ru/ijyhnp A.V. Oksuzyan, E.G. Butolin, M.M. Romashov
Federal State Budgetary Educational Institution of Higher Education “Izhevsk State Medical University”
of the Ministry of health of the Russian Federation, Kommunarov street, 281, Izhevsk, 426034, Russian Federation
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