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Free access | 10.1172/JCI107009

Glycosyltransferases in human blood: II. Study of serum galactosyltransferase and N-acetylgalactosaminyltransferase in patients with liver diseases

Y. S. Kim, J. Perdomo, J. S. Whitehead, and K. J. Curtis

Gastrointestinal Research Laboratory, Veterans Administration Hospital, San Francisco, California 94121

Department of Medicine, University of California School of Medicine, San Francisco, California 94122

Find articles by Kim, Y. in: PubMed | Google Scholar

Gastrointestinal Research Laboratory, Veterans Administration Hospital, San Francisco, California 94121

Department of Medicine, University of California School of Medicine, San Francisco, California 94122

Find articles by Perdomo, J. in: PubMed | Google Scholar

Gastrointestinal Research Laboratory, Veterans Administration Hospital, San Francisco, California 94121

Department of Medicine, University of California School of Medicine, San Francisco, California 94122

Find articles by Whitehead, J. in: PubMed | Google Scholar

Gastrointestinal Research Laboratory, Veterans Administration Hospital, San Francisco, California 94121

Department of Medicine, University of California School of Medicine, San Francisco, California 94122

Find articles by Curtis, K. in: PubMed | Google Scholar

Published August 1, 1972 - More info

Published in Volume 51, Issue 8 on August 1, 1972
J Clin Invest. 1972;51(8):2033–2039. https://doi.org/10.1172/JCI107009.
© 1972 The American Society for Clinical Investigation
Published August 1, 1972 - Version history
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Abstract

Serum galactosyltransferase activity was found to be elevated in patients with alcoholic and other liver disorders but remained at a normal level in patients with a variety of nonhepatic diseases. The properties of the galactosyltransferase in patients with liver disease were compared with those of the enzyme in the serum of normal subjects. The possible presence of inhibitors or activators in the serum was examined. Results indicated that in patients with liver disease, the rise in the serum galactosyltransferase was due to an increase in the level of the enzyme present in normal serum and not due to the appearance of a new enzyme. In the cases examined, the level of the enzyme increased with the deterioration of liver function and declined in a patient recovering from acute alcoholic hepatitis. Another glycosyltransferase, an N-acetylgalactosaminyltransferase, was not elevated in the serum of liver disease patients and, unlike the galactosyltransferase, was not detected in normal liver. The results suggest that the serum galactosyltransferase originates from the liver and that an abnormal rise in the level of this enzyme in serum is due to hepatocellular damage.

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