Female Sprague-Dawley rats were given 0.03% thioacetamide (TAA) in their dr
inking water daily for 4 or 12 weeks, and were then given normal water for
4 weeks after the end of a 12-week TAA treatment to investigate amino acid
metabolism. In the malnourished precirrhotic stage (stage 1) and the malnou
rished cirrhotic stage (stage 2), the aromatic amino acids (AAA), Glu, Asp,
Orn, Arg and Cit increased, and the branched-chain amino acids (BCAA) decr
eased slightly. Because these changes normalized in the well-nourished cirr
hotic stage (stage 3), they might have resulted from impairment of hepatocy
tes and malnutrition. The net uptake of BCAA into the liver increased in st
age 2, but the AAA uptake did not exceed that in normal controls. Portal ve
nous plasma AAA increased to the same level as arterial plasma AAA. These r
esults suggest that the decrease in BCAA was partially due to liver uptake
and that the increase in AAA was induced by reduction of liver uptake and o
verproduction in extrahepatic tissues. The liver contents of BCAA and AAA w
ere unchanged in all stages, so were fury utilized in the impaired liver. T
he increases in Glu, Asp, Orn and Cit might have resulted from overproducti
on in the liver, because these contents of the liver increased in stage 2.
In conclusion, the changes in amino acid metabolism in rats with cirrhosis
induced by TAA closely resemble those seen in human liver cirrhosis. (C) 19
99 Elsevier Science Ireland Ltd. All rights reserved.