NUTRITION DURING PREGNANCY, LACTATION, INFANCY, AND CHILDHOOD
Location: Children Nutrition Research Center (Houston, Tx)
Title: Acute depletion of plasma glutamine increases leucine oxidation in prednisone-treated humans.
| Le Bacquer, Olivier - CENTRE DE RECHERCHE EN NU |
| Mauras, Nelly - NEMOURS CHILDRENS CLINIC |
| Welch, Susan - NEMOURS CHILDRENS CLINIC |
| Darmaun, Dominique - NEMOURS CHILDRENS CLINIC |
Submitted to: Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 27, 2006
Publication Date: April 2, 2007
Citation: Le Bacquer, O., Mauras, N., Welch, S., Haymond, M., Darmaun, D. 2007. Acute depletion of plasma glutamine increases leucine oxidation in prednisone-treated humans. Clinical Nutrition. 26:231-238.
Interpretive Summary: Plasma glutamine is an important amino acid (or building block of body protein) that is thought to have a potential regulatory role in increasing body protein balance. To determine whether the lowering of the plasma glutamine concentration would worsen the negative impact of high dose steroids (corticosteroids) on body protein, seven healthy volunteers received a high dose of oral prednisone (a synthetic but very potent form of the body’s natural steroid, cortisol) for 6 days on 2 separate occasions separated by at least 2 weeks. We conclude that in a model of mild, stress-induced protein loss (steroid administration), a decrease in the plasma concentrations of glutamine per se may worsen branched chain amino acid and protein wasting. These data support a potential role of glutamine in the regulation of protein balance under wasting conditions such as that induced by the administration of high doses of adrenal steroids (cortisol). Further studies will be necessary to determine whether the infusion of glutamine may help improve protein balance in individuals under protein wasting conditions.
To determine whether depletion in plasma glutamine worsens the catabolic response to corticosteroids, seven healthy volunteers received oral prednisone for 6 days on two separate occasions, at least 2 weeks apart, and in random order. On the sixth day of each treatment course, they received 5 h intravenous infusions of L-[1-(14)C]-leucine and L-[1-(13)C]-glutamine in the postabsorptive state (1) under baseline conditions (prednisone only day) and (2) after 24h of treatment with phenylbutyrate (prednisone+phenylbutyrate day), a glutamine chelating agent. Phenylbutyrate treatment was associated with (1) an approximately 15% decline in plasma glutamine concentration (627+/-39 vs. 530+/-31 micromol l(-1); P<0.05), (2) no change in leucine appearance rate, an index of protein breakdown (124+/-9 vs. 128+/-9 micromol kg(-1) h(-1); NS) nor in non-oxidative leucine disposal, an index of whole body protein synthesis (94+/-9 vs. 91+/-7 micromol kg(-1) h(-1); NS), and (3) a approximately 25% rise in leucine oxidation (30+/-1 vs. 38+/-2 micromol kg(-1) h(-1), P<0.05), despite an approximately 25% decline (P<0.05) in leucine concentration. In a model of mild, stress-induced protein catabolism, depletion of plasma glutamine per se may worsen branched chain amino acid and protein wasting.