Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients

Dennis Gore, David L. Chinkes, David W. Hart, Steven Wolf, David Herndon, Arthur P. Sanford

Research output: Contribution to journalArticle

141 Citations (Scopus)

Abstract

Objective: The purpose of this study was to assess if hyperglycemia influences energy expenditure or the extent of muscle protein catabolism in severely burned adults. Design: Retrospective study. Setting: Burn intensive care unit at a university hospital. Patients: Adults with burns on ≥40% of their body surface area. Interventions: Simultaneous measurement of indirect calorimetry and leg net balance of phenylalanine (as an index of muscle protein catabolism). Patients were stratified by plasma glucose values at the time of metabolic measurements (i.e., normal, glucose at ≤130 mg/dL; mild hyperglycemia, glucose at 130-200 mg/dL; severe hyperglycemia, glucose at >200 mg/dL). Measurements and Main Results: Normal (n = 9; plasma glucose, 109 ± 13 mg/dL [mean ± SD]), mildly hyperglycemic (n = 131 plasma glucose, 156 ± 17 mg/dL), and severely hyperglycemic subjects (n = 7, glucose 231 ± 32 mg/dL) were similar in age, body weight, extent of burn area, and daily caloric intake. Severe hyperglycemia was associated with significantly higher arterial concentrations of phenylalanine (normal, 0.079 ± 0.027 μmol/L; severe hyperglycemia, 0.116 ± 0.028; p < .05) and a significantly greater net efflux of phenylalanine from the leg (normal, -0.067 ± 0.072 μmol·min-1·100 mL-1 leg volume; severe hyperglycemia, -0.151 ± 0.080 μmol·min-1·100 mL-1 leg volume; p < .05). Resting energy expenditure and respiratory quotient were similar between patient groups. Conclusions: These findings demonstrate an association between hyperglycemia and an increased rate of muscle protein catabolism in severely burned patients. This suggests a possible link between resistance of muscle to the action of insulin for both glucose clearance and muscle protein catabolism.

Original languageEnglish (US)
Pages (from-to)2438-2442
Number of pages5
JournalCritical Care Medicine
Volume30
Issue number11
StatePublished - Nov 1 2002

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Muscle Proteins
Burns
Hyperglycemia
Glucose
Leg
Phenylalanine
Energy Metabolism
Indirect Calorimetry
Body Surface Area
Energy Intake
Intensive Care Units
Retrospective Studies
Body Weight
Insulin
Muscles

Keywords

  • Energy expenditure
  • Hypermetabolism
  • Insulin resistance
  • Phenylalanine

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Gore, D., Chinkes, D. L., Hart, D. W., Wolf, S., Herndon, D., & Sanford, A. P. (2002). Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients. Critical Care Medicine, 30(11), 2438-2442.

Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients. / Gore, Dennis; Chinkes, David L.; Hart, David W.; Wolf, Steven; Herndon, David; Sanford, Arthur P.

In: Critical Care Medicine, Vol. 30, No. 11, 01.11.2002, p. 2438-2442.

Research output: Contribution to journalArticle

Gore, D, Chinkes, DL, Hart, DW, Wolf, S, Herndon, D & Sanford, AP 2002, 'Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients', Critical Care Medicine, vol. 30, no. 11, pp. 2438-2442.
Gore D, Chinkes DL, Hart DW, Wolf S, Herndon D, Sanford AP. Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients. Critical Care Medicine. 2002 Nov 1;30(11):2438-2442.
Gore, Dennis ; Chinkes, David L. ; Hart, David W. ; Wolf, Steven ; Herndon, David ; Sanford, Arthur P. / Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients. In: Critical Care Medicine. 2002 ; Vol. 30, No. 11. pp. 2438-2442.
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AU - Sanford, Arthur P.

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AB - Objective: The purpose of this study was to assess if hyperglycemia influences energy expenditure or the extent of muscle protein catabolism in severely burned adults. Design: Retrospective study. Setting: Burn intensive care unit at a university hospital. Patients: Adults with burns on ≥40% of their body surface area. Interventions: Simultaneous measurement of indirect calorimetry and leg net balance of phenylalanine (as an index of muscle protein catabolism). Patients were stratified by plasma glucose values at the time of metabolic measurements (i.e., normal, glucose at ≤130 mg/dL; mild hyperglycemia, glucose at 130-200 mg/dL; severe hyperglycemia, glucose at >200 mg/dL). Measurements and Main Results: Normal (n = 9; plasma glucose, 109 ± 13 mg/dL [mean ± SD]), mildly hyperglycemic (n = 131 plasma glucose, 156 ± 17 mg/dL), and severely hyperglycemic subjects (n = 7, glucose 231 ± 32 mg/dL) were similar in age, body weight, extent of burn area, and daily caloric intake. Severe hyperglycemia was associated with significantly higher arterial concentrations of phenylalanine (normal, 0.079 ± 0.027 μmol/L; severe hyperglycemia, 0.116 ± 0.028; p < .05) and a significantly greater net efflux of phenylalanine from the leg (normal, -0.067 ± 0.072 μmol·min-1·100 mL-1 leg volume; severe hyperglycemia, -0.151 ± 0.080 μmol·min-1·100 mL-1 leg volume; p < .05). Resting energy expenditure and respiratory quotient were similar between patient groups. Conclusions: These findings demonstrate an association between hyperglycemia and an increased rate of muscle protein catabolism in severely burned patients. This suggests a possible link between resistance of muscle to the action of insulin for both glucose clearance and muscle protein catabolism.

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