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Dietary Arginine Deficiency Alters Flux of Glutamine and Urea Cycle Intermediates across the Portal-Drained Viscera and Liver of Rats1

Wilburta J. Hartman and Ronald L. Prior2

U.S. Department of Agriculture, Agricultural Research Service, Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111

The effect of an arginine-deficient diet on net flux of amino acids across the portal-drained viscera and across the liver was studied in rats. Blood was obtained after food deprivation and 1 and 2 h after a meal of a 1.0% arginine control diet or an arginine-deficient diet containing 3.4% glutamate. The arginine-deficient diet decreased net portal-drained viscera flux of arginine and increased net portal-drained viscera flux of ornithine and proline. However, net portal-drained viscera flux of citrulline (0.35 ± 0.05 µmol/min) was not influenced by diet; of this rate, 46% (0.16 µmol/min) bypassed the liver and was available for extrahepatic arginine synthesis. However, rats continued to exhibit signs of arginine deficiency such as decreased blood arginine concentrations (by 28%) and increased orotic acid excretion (90-fold). Arterial blood glutamine concentration was 25% higher in rats fed the arginine-deficient diet. In the fed state, net hepatic flux of glutamine was elevated from 0.15 (control) to 1.39 µmol/min, indicating that the liver was a major source of the increased blood glutamine concentrations. Increased production of hepatic glutamine and orotic acid may help rats compensate for dietary arginine deficiency, whereas splanchnic output of citrulline was not increased with dietary arginine deficiency even with a substantial dietary supply of glutamate.


KEY WORDS: • arginine • glutamine • rats • citrulline • glutamate

1 Mention of a trade name, proprietary product or specific equipment does not constitute a guarantee by the U.S. Department of Agriculture and does not imply its approval to the exclusion of other products that may be suitable.

2 To whom correspondence should be addressed.

Manuscript received 28 October 1991. Revision accepted 6 March 1992.




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