title: The effect of prolonged euglycemic hyperinsulinemia on lean body mass after severe burn.
abstract: BACKGROUND
  The hypermetabolic response to burn increases protein catabolism. Euglycemic hyperinsu-linemia with exogenous insulin maintains muscle protein by continued stimulation of net protein synthesis. Our aim was to determine the effect of euglycemic hyperinsulinemia over the entire hospitalization on muscle anabolism by investigating lean body mass (LBM) as the primary endpoint.
  
  
  METHODS
  Eighteen subjects between the ages of 2 and 18 with burns of more than 40% were prospectively randomized into 2 groups, a control (n = 9) and a treatment group (n = 9). The treatment group was given continuous intravenous insulin at a rate of at least 1.5 microU/kg/min to maintain serum glucose levels between 100 to 140 mg/dL. Treatment was instituted 24 to 48 hours after arrival and continued until the patient's injury was 95% healed. All patients received continuous enteral feeding. Patients underwent body composition studies by dual-energy x-ray absorptiometry (DEXA) scan on postoperative day 6 after initial burn excision and when 95% healed.
  
  
  RESULTS
  Nutritional intakes were not different between groups. In the control, subjects continued catabolism resulted in peripheral muscle wasting and centripetal obesity with diminished truncal LBM. The treatment group had improvement in lean body mass (P =.004) and bone mass (P =.025). The treatment group also had less peripheral muscle wasting with overall increases in upper/lower extremity LBM (P =.005). Hospital length of stay in days per percent of total body surface area burned was decreased in the insulin group (control = 1.03 +/- 0.1 vs 0.7 +/- 0.9 for insulin patients; P <.05).
  
  
  CONCLUSIONS
  Euglycemic hyperinsulinemia throughout the hospital course mitigates muscle catabolism and preserves lean body mass.
authors.affiliation: Department of Surgery, University of Texas Medical Branch, and the Shriners Burns Hospital, Galveston 77550, USA.
authors.forename: S J
authors.initials: SJ
authors.lastname: Thomas
authors.forename: K
authors.initials: K
authors.lastname: Morimoto
authors.forename: D N
authors.initials: DN
authors.lastname: Herndon
authors.forename: A A
authors.initials: AA
authors.lastname: Ferrando
authors.forename: R R
authors.initials: RR
authors.lastname: Wolfe
authors.forename: G L
authors.initials: GL
authors.lastname: Klein
authors.forename: S E
authors.initials: SE
authors.lastname: Wolf
mesh_terms: D000328:Adult; D001786:Blood Glucose; D001823:Body Composition; D001835:Body Weight; D002056:Burns / Q000188:drug therapy* / Q000378:metabolism*; D002153:Calorimetry, Indirect; D002648:Child; D002675:Child, Preschool; D004573:Electrolytes / Q000097:blood; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D005260:Female; D005500:Follow-Up Studies; D015309:Glucose Clamp Technique; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D006946:Hyperinsulinism / Q000139:chemically induced / Q000378:metabolism*; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007328:Insulin / Q000008:administration & dosage*; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism; D015596:Nutrition Assessment; D011446:Prospective Studies
chemical_list: D001786:Blood Glucose; D004573:Electrolytes; D007004:Hypoglycemic Agents; D007328:Insulin; D006003:Glycogen