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The prominent role of the liver in the elimination of asymmetric dimethylarginine (ADMA) and the consequences of impaired hepatic function.

Authors
  • Richir, Milan C
  • Bouwman, Roderick H
  • Teerlink, Tom
  • Siroen, Michiel P C
  • de Vries, Theo P G M
  • van Leeuwen, Paul A M
Type
Published Article
Journal
JPEN. Journal of parenteral and enteral nutrition
Publication Date
Jan 01, 2008
Volume
32
Issue
6
Pages
613–621
Identifiers
DOI: 10.1177/0148607108321702
PMID: 18974239
Source
Medline
License
Unknown

Abstract

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS), the enzyme which converts the amino acid arginine into nitric oxide (NO). ADMA has been identified as an important risk factor for cardiovascular diseases. Besides the role of ADMA in cardiovascular diseases, it also seems to be an important determinant in the development of critical illness, (multiple) organ failure, and the hepatorenal syndrome. ADMA is eliminated from the body by urinary excretion, but it is mainly metabolized by the dimethylarginine dimethylaminohydrolase (DDAH) enzymes that convert ADMA into citrulline and dimethylamine. DDAH is highly expressed in the liver, which makes the liver a key organ in the regulation of the plasma ADMA concentration. The prominent role of the liver in the elimination of ADMA and the consequences of impaired hepatic function on ADMA levels will be discussed in this article.

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