Asymmetric Dimethylarginine (ADMA) and other Endogenous Nitric Oxide Synthase (NOS) Inhibitors as an Important Cause of Vascular Insulin Resistance
| Autor: | C. Stefanadis, M. Riga, E. Stefanadi, K. Toutouzas |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
medicine.medical_specialty
Endothelium Endocrinology Diabetes and Metabolism medicine.medical_treatment Clinical Biochemistry Arginine Nitric Oxide Biochemistry Nitric oxide chemistry.chemical_compound Endocrinology Insulin resistance Enos Internal medicine Diabetes mellitus medicine Animals Humans Enzyme Inhibitors Endothelial dysfunction biology business.industry Insulin Biochemistry (medical) General Medicine medicine.disease biology.organism_classification medicine.anatomical_structure chemistry Insulin Resistance Nitric Oxide Synthase Asymmetric dimethylarginine business |
| Zdroj: | Hormone and Metabolic Research. 40:655-659 |
| ISSN: | 1439-4286 0018-5043 |
| DOI: | 10.1055/s-0028-1083814 |
| Popis: | Asymmetric dimethylarginine (ADMA) and NG-monomethyl- L-arginine ( L-NMMA) are important endogenous endothelial nitric oxide synthase (eNOS) inhibitors. Studies have shown that patients with insulin resistance have elevated plasma levels of ADMA. Moreover, ADMA levels have a prognostic value on long-term outcome of patients with coronary artery disease. Insulin resistance, a disorder associated to inadequate biological responsiveness to the actions of exogenous or endogenous insulin, is a metabolic condition, which exists in patients with cardiovascular diseases. This disorder affects the functional balance of vascular endothelium via changes of nitric oxide (NO) metabolism. Nitric oxide is produced in endothelial cells from the substrate L-arginine via eNOS. Elevated ADMA levels cause eNOS uncoupling, a mechanism which leads to decreased NO bioavailability and increased production of hydrogen peroxide. According to clinical studies, the administration of L-arginine to patients with high ADMA levels improves NO synthesis by antagonizing the deleterious effect of ADMA on eNOS function, although in specific populations such as diabetes mellitus, this might even been harmful. More studies are required in order to certify the role of NOS inhibitors in insulin resistance and endothelial dysfunction. It is still difficult to say whether increased ADMA levels in certain populations is only a reason or the result of the molecular alterations, which take place in vascular disease states. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|