Article Text

  1. S Verbruggen1,
  2. J Coss-Bu3,
  3. K Joosten1,
  4. J van Goudoever1,
  5. L Castillo1
  1. 1Pediatrics Department, Erasmus MC, Sophia Children’s Hospital, Rotterdam, The Netherlands,
  2. 2Children’s Nutrition Research Center, Baylor College of Medicine, Houston, Texas, USA,
  3. 3Intensive Care Unit, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas, USA


Objective: To determine whether a higher protein intake will improve the protein balance (synthesis—breakdown) in septic children under conditions of a hyperinsulinaemic euglycaemic clamp (HEC).

Methods: Six septic adolescents on total parenteral nutrition (age 15 ± 1 years; body mass index 23 ± 4 kg/m2) were studied twice and randomly assigned to receive either standard (1.4 ± 0.2 g/kg per day) or high (2.8 ± 0.4 g/kg per day) protein intake based on age. The subjects received a primed, constant, 7 h tracer infusion of l-[1-13C] leucine and [6,6-2H2] glucose. During the last 3 h of the tracer study we conducted a HEC starting with 80 mU/m2 per minute insulin infusion. Plasma glucose was clamped during the last 30 minutes at 98 ± 6 mg/dl. Blood samples were obtained for determination of plasma isotopic enrichment.

Results: Glucose rates of appearance during HEC were 22 ± 4 and 26 ± 5 μmol/kg per minute (p = 0.15), respectively, for standard and high protein intakes. Insulin sensitivity was approximately 0.2 μmol/kg per minute per μU/ml at standard and high protein intake. During baseline, protein balance at standard protein intake was 0.1 ± 0.3 versus 0.8 ± 0.5 g/kg per day at high protein intake (p = 0.06). During HEC protein balance at standard protein intake was 0.2 ± 0.4 versus 0.8 ± 0.5 g/kg per day with high protein intake (p = 0.07).

Conclusions: These preliminary data show insulin resistance in critically ill children. Higher protein intake slightly improved whole body protein balance. However, insulin did not appear to improve protein balance further. Glucose turnover rates increased with high protein intake, which may correspond to increased gluconeogenesis.

NIH DK-62363, T32 HD-007445, Ajinomoto 3-ARP; USDA/ARS 25337387.

Sophia Foundation Scientific Research (SSWO).

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