Glutamine kinetics in burn patients. Comparison with hormonally induced stress in volunteers
D. C. Gore and F. Jahoor
Department of Surgery, Medical College of Virginia, Richmond.
OBJECTIVE: To assess the acute and protracted adaptive response of
peripheral glutamine kinetics to a severe injury. DESIGN: Comparison study.
SETTING: Clinical research center at a university-affiliated hospital.
PATIENTS: Six severely burned men and five young healthy men.
INTERVENTIONS: The catabolic hormones epinephrine, cortisol, and glucagon
were infused simultaneously into the femoral artery of five healthy
volunteers, thus acutely simulating the hormonal milieu associated with a
severe injury. MAIN OUTCOME MEASURES: Whole-body glutamine flux and
peripheral glutamine kinetics were determined using glutamine labeled with
nitrogen 15 and net balance measurements in patients 2 weeks following a
severe burn injury. Identical measurements were made in the healthy
volunteers before and following 4 hours of catabolic hormone infusion.
RESULTS: Whole-body glutamine flux increased to a similar extent in both
the burn patients and in volunteers following catabolic hormone infusion.
In comparison with their basal kinetics, the hormonally simulated acute
stress in the volunteers induced a significant efflux of glutamine from the
leg by greatly increasing the rate of glutamine appearance. In contrast,
burn patients had a significant decrease in their rate of glutamine
appearance and achieved a similar net loss of glutamine from the leg only
by a compensatory decrease in peripheral glutamine consumption.
CONCLUSIONS: These findings suggest that in the acute stress response,
skeletal muscle preferentially releases glutamine from its free
intracellular pool. As this reserve becomes depleted, net glutamine efflux
is maintained by decreasing its rate of muscle glutamine utilization. These
results suggest a failure of muscle to augment de novo glutamine synthesis
and support the conclusion that glutamine is a conditionally essential
amino acid during critical illness.
Corticosteroids increase glutamine utilization in human splanchnic bed
Thibault et al.
Am. J. Physiol. Gastrointest. Liver Physiol. 2008;294:G548-G553.
ABSTRACT
| FULL TEXT
Glutamine kinetics and protein turnover in end-stage renal disease
Raj et al.
Am. J. Physiol. Endocrinol. Metab. 2005;288:E37-E46.
ABSTRACT
| FULL TEXT
Amino Acid Adequacy in Pathophysiological States
Soeters et al.
J. Nutr. 2004;134:1575S-1582S.
ABSTRACT
| FULL TEXT
Parenteral Glutamine Supplementation Does Not Reduce the Risk of Mortality or Late-Onset Sepsis in Extremely Low Birth Weight Infants
Poindexter et al.
Pediatrics 2004;113:1209-1215.
ABSTRACT
| FULL TEXT
Effects of glutamine supplementation, GH, and IGF-I on glutamine metabolism in critically ill patients
Jackson et al.
Am. J. Physiol. Endocrinol. Metab. 2000;278:E226-E233.
ABSTRACT
| FULL TEXT
Inactivity Amplifies the Catabolic Response of Skeletal Muscle to Cortisol
FERRANDO et al.
J. Clin. Endocrinol. Metab. 1999;84:3515-3521.
ABSTRACT
| FULL TEXT
The metabolic consequences of critical illness: acute effects on glutamine and protein metabolism
Jackson et al.
Am. J. Physiol. Endocrinol. Metab. 1999;276:E163-E170.
ABSTRACT
| FULL TEXT
Pharmacological Nutrition After Burn Injury
De-Souza and Greene
J. Nutr. 1998;128:797-803.
ABSTRACT
| FULL TEXT
Glutamine and leucine nitrogen kinetics and their relation to urea nitrogen in newborn infants
Parimi et al.
Am. J. Physiol. Endocrinol. Metab. 2002;282:E618-E625.
ABSTRACT
| FULL TEXT