In acute CCI(4), intoxication of rats significantly increased activities of hepatic
low-K(m) hexokinases, glucose-6-phosphate dehydrogenase, phosphofructokinase, aldolase
A and pyruvate kinase M(2) with concurrently decreased activities of glucokinase, glucose-
6-phosphatase, fructose-1,6-diphosphatase, aldolase B and pyruvate kinase L were observed.
The resulting enzyme pattern was apparently different from that in dietary induction.
Principal component analysis revealed that the degree of enzyme deviation in the injured
liver was much greater than that in the regenerating liver after partial hepatectomy and
was closer to that in fetal liver or hepatoma tissue.
Activities of key carbohydrate-metabolizing enzymes were determined on
biopsied liver tissues obtained from patients with acute and chronic viral hepatitis and
postnecrotic cirrhosis of the liver. The results indicated that the activities of fetal or prototype
enzymes, low-K(m) hexokinases, glucose-6-phosphate dehydrogenase and pyruvate
kinase type M(2) increased, while those of adult type liver enzymes, glucokinase, glucose-6-
phosphatase, fructose-1, 6-diphosphatase and pyruvate kinase type L decreased in livers
of these cases. Phosphofructokinase activity tended to increase only in acute hepatitis.
Principal component analysis revealed that the enzyme patterns of acute hepatitis and liver
cirrhosis were most deviated from the control and closely resembled those of hepatocellular
carcinomas.
Glucagon effectively prevented the increase in glucose-6-phosphate dehydrogenase
activity of rat liver following the administration of a glucose-casein mixture without
altering the amount of the diet consumed. However, the increase of the enzyme level in
carbon tetrachloride-injured rat liver was virtually insensitive to glucagon. The results
obtained gave further evidence for the difference between these two induction mechanisms
of glucose-6-phosphate dehydrogenase.
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