Enteral glutamine spares endogenous glutamine in chronic acidosis.

Metabolic acidosis associated with the catabolic state mobilizes muscle nitrogen and releases it into blood as glutamine (GLN) targeted for renal consumption and base generation. Because GLN removed by the kidneys during acidosis is a major drain on the GLN available to other sites, subsequent deprivation may lead to impaired organ function. Conversely, GLN supplementation may spare endogenous supplies and restore organ function. To test this, Sprague-Dawley rats weighing between 250 and 350 g were pair-fed elemental diets supplemented with GLN 4.9 g/L (GLN-ED) or an equivalent mixture of neutral amino acids substituted for GLN (ED). Acid loading was effected by adding hydrochloric acid to the liquid diet (110 mmol/L). Animals were studied in metabolic cages for five consecutive 24-hour urine collection periods and then anesthetized for short-term studies of interorgan fluxes and tissue GLN content. Acidosis effected an increase in ammonium nitrogen excretion (fivefold) and a reciprocal decrease (24%) in urea nitrogen excretion. Enteral GLN had no effect on the acidosis-effected ammonium (2170 +/- 71 vs 2059 +/- 361 mumol/100 g, ED vs GLN-ED, respectively) or urea excretion (5522 +/- 95 vs 5915 +/- 984 mumol/100 g, ED vs GLN-ED, respectively). Although arterial blood GLN was not increased in the GLN-ED group (531 +/- 58 vs 438 +/- 51 nmol/mL, p = .10), both liver and muscle GLN were elevated (11,650 +/- 1137 nmol/g vs 7063 +/- 578 and 5503 +/- 489 and 4742 +/- 333 nmol/g, respectively, each p < .05).(ABSTRACT TRUNCATED AT 250 WORDS)