Open AccessAsymmetric dimethylarginine and the effect of folate substitution in children with familial hypercholesterolemia and diabetes mellitus type 1
Author(s) -
Petr Jehlička,
F Stožický,
Otto Mayer,
J Varvařovská,
Jaroslav Ráček,
Ladislav Trefil,
Konrad Siala
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931418
Subject(s) - asymmetric dimethylarginine , medicine , homocysteine , endocrinology , endothelial dysfunction , diabetes mellitus , familial hypercholesterolemia , type 2 diabetes mellitus , arginine , cholesterol , amino acid , chemistry , biochemistry
A recently discussed cardiovascular risk factor, asymmetricdimethylarginine (ADMA), is known to act as an endogenousinhibitor of endothelial nitric oxide synthase. The aim of thisstudy was to establish 1) the relationship between ADMA andultrasonographically or biochemically determined endothelialdysfunction in children, and 2) the effect of folatesupplementation on these parameters. The study cohort included32 children with familial hypercholesterolemia (FH), 30 withdiabetes mellitus type 1 (DM1) and 30 age-matched healthychildren as the control group. Furthermore, twenty-eightrandomly selected FH and DM1 children were re-examined after3-months supplementation with folic acid. Baseline levels ofADMA and oxidized low density lipoproteins (oxLDL) weresignificantly higher in FH group than in DM1 and healthy children.Children in DM1 group had significantly lower concentration ofhomocysteine, but ADMA levels were normal. Folic acidsupplementation significantly lowered homocysteine and hsCRPlevels in both FH and DM1 group; however, ADMA and oxLDLconcentrations remained unaltered. In conclusion, ADMA andoxLDL appear to be associated with endothelial dysfunction inchildren with FH. Administration of folic acid did not influencethese markers in both FH and DM1 children.