title: Defective remethylation of homocysteine is related to decreased synthesis of coenzymes B2 in thyroidectomized rats.
abstract: We investigated the influence of hypothyroidism on homocysteine metabolism in rats, focusing on a hypothetical deficient synthesis of FAD by riboflavin kinases. Animals were allocated in control group (n = 7), thyroidectomized rats (n = 6), rats with diet deficient in vitamin B2, B9, B12, choline and methionine (n = 7), thyroidectomized rats with deficient diet (n = 9). Homocysteine was decreased in operated rats (2.6 +/- 1.01 vs. 4.05 +/- 1.0 mumol/L, P = 0.02) and increased in deficient diet rats (29.56 +/- 4.52 vs. 4.05 +/- 1.0 micromol/L, P = 0.001), when compared to control group. Erythrocyte-Glutathione-Reductase-Activation-Coefficient (index of FAD deficiency) was increased in thyroidectomized or deficient diet rats (P = 0.004 for both). Methylenetetrahydrofolate-reductase and methionine-synthase activities were decreased in thyroidectomized rats but not in those subjected to deficient diet. Cystathionine-beta-synthase was increased only in operated rats. Taken together, these results showed a defective re-methylation in surgical hypothyroidism, which was due in part to a defective synthesis of vitamin B2 coenzymes. This defective pathway was overcompensated by the increased Cystathionine-beta-synthase activity.
authors.affiliation: Laboratory of Cellular and Molecular Pathology in Nutrition, INSERM-0014, Medical Faculty, University of Nancy I, 54500 Vandoeuvre lès Nancy, France.
authors.forename: A
authors.initials: A
authors.lastname: Ayav
authors.forename: J M
authors.initials: JM
authors.lastname: Alberto
authors.forename: F
authors.initials: F
authors.lastname: Barbe
authors.forename: L
authors.initials: L
authors.lastname: Brunaud
authors.forename: P
authors.initials: P
authors.lastname: Gerard
authors.forename: M
authors.initials: M
authors.lastname: Merten
authors.forename: J L
authors.initials: JL
authors.lastname: Gueant
mesh_terms: D013766:5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / Q000096:biosynthesis / Q000378:metabolism; D000818:Animals; D003541:Cystathionine beta-Synthase / Q000096:biosynthesis / Q000378:metabolism; D004032:Diet; D004798:Enzymes / Q000096:biosynthesis* / Q000187:drug effects / Q000378:metabolism; D004912:Erythrocytes / Q000187:drug effects / Q000201:enzymology; D005978:Glutathione / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood / Q000187:drug effects; D006710:Homocysteine / Q000378:metabolism*; D007037:Hypothyroidism / Q000378:metabolism*; D008297:Male; D008745:Methylation; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000096:biosynthesis / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344; D012044:Regression Analysis; D012256:Riboflavin / Q000378:metabolism*; D013965:Thyroidectomy / Q000009:adverse effects; D014806:Vitamin B 12 Deficiency / Q000378:metabolism
chemical_list: D004798:Enzymes; D006710:Homocysteine; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D005980:Glutathione Reductase; D013766:5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; D003541:Cystathionine beta-Synthase; D005978:Glutathione; D012256:Riboflavin