NDLI: Interorgan ammonia trafficking in liver disease

Content Provider	Springer Nature Link
Author	Olde Damink, Steven W. M. Jalan, Rajiv Dejong, Cornelius H. C.
Copyright Year	2008
Abstract	Patients with liver disease have reduced urea synthesis capacity resulting in reduced capacity to detoxify ammonia in the liver. The contribution of the gut to the hyperammonemic state observed during liver failure is mainly due to portacaval shunting and not the result of changes in the metabolism of ammonia in the gut. Small intestinal synthesis of ammonia is related to amino acid breakdown, predominantly glutamine, whereas large bowel ammonia production is caused by bacterial breakdown of amino acids and urea. The kidneys produce ammonia but adapt to liver failure in experimental portacaval shunting by reducing ammonia release into the systemic circulation. The kidneys have the ability to switch from net ammonia production to net ammonia excretion. Data from recent studies in patients with cirrhosis of the liver show that the kidneys have a major role in post upper gastrointestinal bleeding hyperammonemia. During hyperammonemia muscle takes up ammonia and plays a major role in (temporarily) detoxifying ammonia to glutamine. Net uptake of ammonia by the brain occurs in patients and experimental animals with acute and chronic liver failure. Insight will be given in recent developments on ammonia lowering therapies which are based on the information of interorgan ammonia trafficking.
Starting Page	169
Ending Page	181
Page Count	13
File Format	PDF
ISSN	08857490
Journal	Metabolic Brain Disease
Volume Number	24
Issue Number	1
e-ISSN	15737365
Language	English
Publisher	Springer US
Publisher Date	2008-12-09
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Ammonia Glutamine Interorgan metabolism Liver failure Cirrhosis Oncology Biochemistry Neurology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Biochemistry Neurology (clinical) Cellular and Molecular Neuroscience

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