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Department of Physiology, Louisiana State University Medical Center, Shreveport, LA 71130
Enteral glutamine feeding effect on renal glutamine utilization was assessed from the perspective of gamma glutamyltransferase activity-dependent cellular glutamate modulation of phosphate-dependent glutaminase. After 4 d, rats fed an elemental diet supplemented with glutamine exhibited a 21% higher kidney glutamate content and 27% reduction in ammonium excretion, both P < 0.05. Glutamine removal from plasma was depressed 62% in the glutamine-fed group (324 ± 155 vs. 780 ± 154 nmol·min-1·100 g body weight-1, P < 0.05) despite an elevated arterial plasma glutamine load delivered to the kidney. Administration of acivicin, 36 mg/kg body weight, to glutamine-fed rats inhibited gamma glutamyltransferase > 90% and decreased kidney glutamate content 42%. This reduction in kidney glutamate was associated with a 3.3-fold enhancement in both glutamine extraction (474 ± 184 to 1548 ± 255 nmol·min-1·100 g body weight-1) and ammonium excretion (295 ± 30 to 978 ± 96 nmol·min-1·100 g body weight-1), both P < 0.01. These findings are consistent with enteral glutamine regulation of renal glutamine utilization through an elevation of the cellular glutamate level.
KEY WORDS: rat enteral glutamine glutamine utilization ammonium excretion cellular glutamate gamma glutamyltransferase
1 Presented as part of the Symposium: "Glutamine Nutrition and Metabolism: Bridging Clinical Medicine and Basic Science" given at the Experimental Biology '95 meeting, Atlanta, GA, on April 13, 1995. This symposium was sponsored by the American Institute of Nutrition and supported in part by Ross Laboratories. Guest editor for the symposium publication was Josef Neu, University of Florida, Gainesville, FL.
2 To whom correspondence should be addressed: Department of Physiology, Louisiana State University Medical Center, P.O. Box 33932, 1501 Kings Highway, Shreveport, LA 71130.
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