title: The influence of methionine, selenomethionine, and vitamin E on liver metabolic pathways and steatosis in high-cholesterol fed rabbits.
abstract: Significant disorders of liver metabolic pathways enzymes after high-cholesterol diet could give information on liver steatosis development. This process could probably also be inhibited by some compounds, as examined in rabbits. Forty-two male rabbits were served a high-cholesterol diet (2 g%) (0.67 g/kg b.m./24 h) with addition of d,l-methionine (70 mg/kg b.m./24 h) or seleno-d,l-methionine (12.5 microg/kg b.m./24 h) or alpha-tocopherol (10 mg/kg b.m./24 h) for 3 months to compare the protection effect of used compounds on liver metabolism and steatosis. At the beginning and every month, blood was taken. After the experiment was completed, livers were dissected for histological examinations. The concentration of total cholesterol (t-CH), triacylglycerol (TG), and the activities of aldolase (ALD), sorbitol dehydrogenase (SDH), glutamate dehydrogenase (GLDH), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were determined. Plasma t-CH and TG concentrations were significantly higher in all experimental groups vs control group. Blood serum AST and ALT activities did not undergo change but there were observed not significant increase in the CH group vs control group. Activities of SDH, GLDH, and LDH increased in blood serum and decreased in the liver in all experimental groups. Activities of LDH and SDH increased in the liver in the CH+Met group vs CH group. ALD activity decreased in the liver only in the CH and CH+Se groups. This data support a lipotoxic model of cholesterol-mediated hepatic steatosis. Prolonged administration of high-cholesterol diet not only disturbs the structure of cell membranes, which is expressed by decreased activity of enzymes in the liver and the migration of those enzymes to plasma but as well leads to steatosis of the liver, which has been confirmed by histological examinations. The applied compounds appear to have a varying influence upon the activity of enzymes determined in serum and liver. Obtained results showed a beneficial influence of methionine and vitamin E supplementation on liver steatosis development.
authors.affiliation: Department of Biochemistry in Zabrze, Medical University of Silesia, Katowice, Poland.
authors.forename: Ewa
authors.initials: E
authors.lastname: Birkner
authors.forename: Jolanta
authors.initials: J
authors.lastname: Zalejska-Fiolka
authors.forename: Aleksandra
authors.initials: A
authors.lastname: Kasperczyk
authors.forename: Sławomir
authors.initials: S
authors.lastname: Kasperczyk
authors.forename: Ewa
authors.initials: E
authors.lastname: Grucka-Mamczar
authors.forename: Barbara
authors.initials: B
authors.lastname: Stawiarska-Pieta
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Birkner
mesh_terms: D000410:Alanine Transaminase; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000008:administration & dosage*; D005234:Fatty Liver / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D005634:Fructose-Bisphosphate Aldolase / Q000378:metabolism; D005969:Glutamate Dehydrogenase / Q000378:metabolism; D007064:L-Iditol 2-Dehydrogenase / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008715:Methionine / Q000494:pharmacology*; D011817:Rabbits; D012645:Selenomethionine / Q000494:pharmacology*; D014280:Triglycerides / Q000097:blood; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D002791:Cholesterol, Dietary; D014280:Triglycerides; D014810:Vitamin E; D012645:Selenomethionine; D002784:Cholesterol; D008715:Methionine; D007064:L-Iditol 2-Dehydrogenase; D007770:L-Lactate Dehydrogenase; D005969:Glutamate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005634:Fructose-Bisphosphate Aldolase