American Journal of Clinical Nutrition, Vol 14, 302-309, Copyright © 1964 by The American Society for Clinical Nutrition, Inc.

Studies of Rat Liver and Kidney Enzymes

II. Response to Dietary Protein Deficiency and Repletion During Chronic Administration of Ammonium Acetate and l-Glutamine

¹ From the Department of Medicine, Division of Diabetes and Metabolism, University of Oregon Medical School, Portland, Oregon

Ingestion of deficient amounts of dietary protein (8 per cent casein) produced a marked failure of weight gain in weanling rats from zero to six weeks and resulted in a decrease of the specific activities of all liver and kidney enzymes measured at three weeks (carbamyl phosphate synthetase, ornithine transcarbamylase, arginine synthetase, arginase, glutamotransferase, l-glutamic dehydrogenase and glutamic oxaloacetic transaminase) except kidney arginase which was increased but not significantly. Continued dietary protein deficiency to six weeks resulted in a less severe repression of enzyme activities (a return toward control values), and liver carbamyl phosphate synthetase activity was actually increased as a result of extending the protein-deficient diet an additional three weeks. This suggests the attainment of adaptive equilibrium.

Both intragastric ammonium acetate and l-glutamine when administered to young rats (zero to three weeks) receiving a protein-deficient diet prevented the enzyme repressions observed with dietary protein deficiency alone with the exception of liver glutamotransferase. Ammonium acetate increased liver glutamicoxaloacetic transaminase activity, and l-glutamine increased liver carbamyl phosphate synthetase activity. These observations suggest that ammonium acetate and l-glutamine or nitrogen are capable of substituting for certain enzyme substrates when normal dietary protein is lacking. Ammonium acetate and l-glutamine administration was not as effective in the older (three to six week) rats in preventing the enzyme repressions observed from deficient dietary protein alone.

Protein repletion as measured by the enzyme response of liver ornithine transcarbamylase, arginine synthetase, glutamotransferase and kidney arginine synthetase and glutamotransferase prevented the enzyme repressions observed in six week rats receiving a protein-deficient diet alone. Liver ornithine transcarbamylase and kidney arginine synthetase were markedly induced, and the increase of liver carbamyl phosphate synthetase activity from protein deficiency alone was prevented by protein repletion. Liver glutamic oxaloacetic transaminase was repressed, and liver arginase and l-glutamic dehydrogenase did not respond to protein repletion suggesting that the level of these enzymes is controlled in a different manner.

Both ammonium acetate and l-glutamine given with the protein repletion diet were similar in effect as compared to a protein repletion diet alone. Kidney glutamotransferase, however, was increased with both ammonium acetate and l-glutamine, and kidney glutamic oxaloacetic transaminase decreased with l-glutamine but not ammonium acetate administration. l-Glutamine given with the protein repletion diet increased both liver and kidney arginine synthetase activity more effectively than did ammonium acetate given with the protein repletion diet, or the protein repletion diet alone.