A. Mühl
Research Subjects
A. Mühl has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Burkhard Simma
Department of Pediatrics, Academic Teaching Hospital, Landeskrankenhaus Feldkirch, Feldkirch, Austria
1 shared publication - D. Mayr
Department of Pediatrics Landeskrankenhaus Bregenz Carl Pedenz Str. 2 Bregenz 6900 Austria
1 shared publication - Dorothea Möslinger
Department of Paediatrics and Adolescent Medicine, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria
1 shared publication - Hanno Ulmer
Institute of Clinical Epidemiology, Public Health, Health Economics, Medical Statistics and Informatics, Medical University of Innsbruck, Innsbruck 6020, Austria
1 shared publication - I. Schmid
University Institute for Clinical Chemistry Müllner Hauptstraße 48 Salzburg 5020 Austria
1 shared publication - Martina Huemer
Division of Metabolism and Children's Research Centre University Children's Hospital Zurich, University of Zurich Zurich Switzerland
1 shared publication
Latest Publications
- 31 January 2012
- Published by Wiley in Journal of Inherited Metabolic Disease
- Vol. 35 (5) , 817-821
Free asymmetric dimethylarginine (ADMA) is low in children and adolescents with classical phenylketonuria (PKU)
Introduction: Free asymmetric dimethylarginine (ADMA) is a competitive inhibitor of the nitric oxide synthases (NOS). Suppression of nitric oxide (NO) synthesis increases the risk of atherosclerosis. Nevertheless, in the condition of oxidative stress, NOS blockade by ADMA may exert protective effects. Protein metabolism is altered in patients with phenylketonuria (PKU) on dietary treatment and as shown recently, oxidative stress is high in PKU. Since free ADMA concentrations are determined by both protein metabolism and oxidative stress we hypothesized, that free ADMA levels may be elevated in PKU patients.Design: Sixteen patients with PKU on dietary treatment (mean age 10.1 ± 5.2 yrs), and 91 healthy children (mean age 11.6 ± 3.7 yrs) participated in a cross sectional study.Results: ADMA, total homocysteine (tHcy) and blood glucose were lower and the L‐arginine/ADMA ratio was higher in PKU patients compared to controls. No significant correlation was present between phenylalanine (Phe) concentrations, protein intake, and lipid profile, history of cardiovascular disease or ADMA.Discussion: In contrast to our hypothesis, ADMA was lower and the L‐arginine/ADMA ratio was higher in PKU patients. Therefore, in PKU patients, the regulating function of ADMA on NO synthesis is altered and may thus contribute to oxidative stress.
- 31 January 2012
- Published by Wiley in Journal of Inherited Metabolic Disease
- Vol. 35 (5) , 817-821
Free asymmetric dimethylarginine (ADMA) is low in children and adolescents with classical phenylketonuria (PKU)
Introduction: Free asymmetric dimethylarginine (ADMA) is a competitive inhibitor of the nitric oxide synthases (NOS). Suppression of nitric oxide (NO) synthesis increases the risk of atherosclerosis. Nevertheless, in the condition of oxidative stress, NOS blockade by ADMA may exert protective effects. Protein metabolism is altered in patients with phenylketonuria (PKU) on dietary treatment and as shown recently, oxidative stress is high in PKU. Since free ADMA concentrations are determined by both protein metabolism and oxidative stress we hypothesized, that free ADMA levels may be elevated in PKU patients.Design: Sixteen patients with PKU on dietary treatment (mean age 10.1 ± 5.2 yrs), and 91 healthy children (mean age 11.6 ± 3.7 yrs) participated in a cross sectional study.Results: ADMA, total homocysteine (tHcy) and blood glucose were lower and the L‐arginine/ADMA ratio was higher in PKU patients compared to controls. No significant correlation was present between phenylalanine (Phe) concentrations, protein intake, and lipid profile, history of cardiovascular disease or ADMA.Discussion: In contrast to our hypothesis, ADMA was lower and the L‐arginine/ADMA ratio was higher in PKU patients. Therefore, in PKU patients, the regulating function of ADMA on NO synthesis is altered and may thus contribute to oxidative stress.