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Asymmetric dimethylarginine and the effect of folate substitution in children with familial hypercholesterolemia and diabetes mellitus type 1
Petr Jehlička, František Stožický, Otto Mayer Jr., Jana Varvařovská, Jaroslav Racek, Ladislav Trefil, K. Siala
Language English Country Czech Republic
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- MeSH
- Anticholesteremic Agents administration & dosage MeSH
- Arginine analogs & derivatives blood MeSH
- Azetidines administration & dosage MeSH
- Biomarkers blood MeSH
- Endothelium, Vascular metabolism drug effects ultrasonography MeSH
- Diabetes Mellitus, Type 1 metabolism MeSH
- Child MeSH
- Financing, Organized MeSH
- Hyperlipoproteinemia Type II epidemiology drug therapy metabolism MeSH
- Drug Therapy, Combination MeSH
- Folic Acid administration & dosage MeSH
- Humans MeSH
- Lipoproteins, LDL blood MeSH
- Adolescent MeSH
- Risk Factors MeSH
- Hydroxymethylglutaryl-CoA Reductase Inhibitors administration & dosage MeSH
- Vitamin B Complex administration & dosage MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Female MeSH
A recently discussed cardiovascular risk factor, asymmetric dimethylarginine (ADMA), is known to act as an endogenous inhibitor of endothelial nitric oxide synthase. The aim of this study was to establish 1) the relationship between ADMA and ultrasonographically or biochemically determined endothelial dysfunction in children, and 2) the effect of folate supplementation on these parameters. The study cohort included 32 children with familial hypercholesterolemia (FH), 30 with diabetes mellitus type 1 (DM1) and 30 age-matched healthy children as the control group. Furthermore, twenty-eight randomly selected FH and DM1 children were re-examined after 3-months supplementation with folic acid. Baseline levels of ADMA and oxidized low density lipoproteins (oxLDL) were significantly higher in FH group than in DM1 and healthy children. Children in DM1 group had significantly lower concentration of homocysteine, but ADMA levels were normal. Folic acid supplementation significantly lowered homocysteine and hsCRP levels in both FH and DM1 group; however, ADMA and oxLDL concentrations remained unaltered. In conclusion, ADMA and oxLDL appear to be associated with endothelial dysfunction in children with FH. Administration of folic acid did not influence these markers in both FH and DM1 children.
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Lit.: 18
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- $a 10.33549/physiolres.931418 $2 doi
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- $a Department of Pediatrics, Charles University in Prague, Plzeň JEHLICKA@fnplzen.cz
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- $a Lit.: 18
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- $a A recently discussed cardiovascular risk factor, asymmetric dimethylarginine (ADMA), is known to act as an endogenous inhibitor of endothelial nitric oxide synthase. The aim of this study was to establish 1) the relationship between ADMA and ultrasonographically or biochemically determined endothelial dysfunction in children, and 2) the effect of folate supplementation on these parameters. The study cohort included 32 children with familial hypercholesterolemia (FH), 30 with diabetes mellitus type 1 (DM1) and 30 age-matched healthy children as the control group. Furthermore, twenty-eight randomly selected FH and DM1 children were re-examined after 3-months supplementation with folic acid. Baseline levels of ADMA and oxidized low density lipoproteins (oxLDL) were significantly higher in FH group than in DM1 and healthy children. Children in DM1 group had significantly lower concentration of homocysteine, but ADMA levels were normal. Folic acid supplementation significantly lowered homocysteine and hsCRP levels in both FH and DM1 group; however, ADMA and oxLDL concentrations remained unaltered. In conclusion, ADMA and oxLDL appear to be associated with endothelial dysfunction in children with FH. Administration of folic acid did not influence these markers in both FH and DM1 children.
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