Branched chain amino acids in heptatic encephalopathy.
BACKGROUND
Early theories or hepatic encephalopathy focused on ammonia-driven disruption of the Krebs cycle and cellular energy production. The "false-neurotransmitter" theory directed attention toward the interactions of amino acids, metabolism, the blood-brain barrier and neurotransmission. As they evolved, these studies revealed surprising and subtle effects of ammonia on brain amino acid uptake.


METHODS
Research over a 15-year period in Josef E. Fischer's laboratory explored many aspects of these interactions. Subsequent studies by others have confirmed and extended them into other areas. Insights from this work continue to stimulate attempts to confirm or disprove the clinical utility of branched chain amino acids.


CONCLUSIONS
Increased understanding of the factors affecting ammonia, amino acid and neurotransmitter disturbances in chronic liver failure have made a significant and ongoing contribution to the study of metabolism in health and disease.
James
J Howard
JH
Department of Surgery, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0558, USA. james.james@uc.edu
D027062:Amino Acid Transport System L / Q000378:metabolism*; D000597:Amino Acids, Branched-Chain / Q000378:metabolism*; D000641:Ammonia / Q000097:blood*; D000818:Animals; D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D006501:Hepatic Encephalopathy / Q000097:blood / Q000378:metabolism*; D006801:Humans; D012701:Serotonin / Q000378:metabolism
D027062:Amino Acid Transport System L; D000597:Amino Acids, Branched-Chain; D005973:Glutamine; D012701:Serotonin; D000641:Ammonia; D004298:Dopamine