Cerebral energy metabolism in hepatic encephalopathy and hyperammonemia.

Abstract:

:Hepatic encephalopathy (HE) is an important cause of morbidity and mortality in patients with severe liver disease. Although the molecular basis for the neurological disorder in HE remains elusive, elevated ammonia and its chief metabolite glutamine are believed to be important factors responsible for altered cerebral functions, including multiple neurotransmitter system(s) failure, altered bioenergetics, and more recently oxidative stress. Accumulated evidence suggests that direct interference of ammonia at several points in cerebral energy metabolism, including glycolysis, TCA cycle, and the electron transport chain, could lead to energy depletion. Additionally, recent studies from our laboratory have invoked the possibility that ammonia and glutamine may induce the mitochondrial permeability transition in astrocytes, a process capable of causing mitochondrial dysfunction. Altered mitochondrial metabolism appears to be an important mechanism responsible for the cerebral abnormalities associated with HE and other hyperammonemic states.

journal_name

Metab Brain Dis

journal_title

Metabolic brain disease

authors

Rao KV,Norenberg MD

doi

10.1023/a:1011666612822

subject

Has Abstract

pub_date

2001-06-01 00:00:00

pages

67-78

issue

1-2

eissn

0885-7490

issn

1573-7365

journal_volume

16

pub_type

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