• Marijke Gielen, Dieter Mesotten, Michael Brugts, Willy Coopmans, Erik Van Herck, Ilse Vanhorebeek, Robert Baxter, Steven Lamberts, Joop A M J L Janssen, and Greet Van den Berghe.
• Department and Laboratory of Intensive Care Medicine, Katholieke Universiteit Leuven, B-3000 Leuven, Belgium.
• J. Clin. Endocrinol. Metab. 2011 Aug 1;96(8):2558-66.

ContextIntensive insulin therapy (IIT) improved outcome in the adult and pediatric intensive care unit (PICU) compared with conventional insulin therapy (CIT). IIT did not increase the anabolic hormone IGF-I in critically ill adults, but feeding in critically ill children and pediatric hormonal responses may differ. Twenty-five percent of the children with IIT experienced hypoglycemia, which may have evoked counterregulatory responses.ObjectiveWe hypothesized that IIT reactivates the somatotropic axis and anabolism in PICU patients.DesignThis was a preplanned subanalysis of a randomized controlled trial on IIT.PatientsWe studied 369 patients who stayed in PICU for at least 3 d (study 1) and 126 patients in a nested case-control study (study 2).Main Outcome MeasuresCirculating insulin, C-peptide, GH, IGF-I, bioavailable IGF-I, IGF-binding protein (IGFBP)-1, IGFBP-3, and acid-labile subunit were analyzed upon admission and d 3. In the nested case-control study, the somatotropic axis, cortisol, and glucagon were analyzed before and after hypoglycemia.ResultsOn d 3, C-peptide was more than 10-fold lower (P < 0.0001) in the IIT group than in the CIT group. IIT increased circulating GH (P = 0.04) and lowered bioavailable IGF-I (P = 0.002). IIT also decreased IGFBP-3 (P = 0.0005) and acid-labile subunit (P = 0.007), while increasing IGFBP-1 (P = 0.04) and the urea/creatinine ratio, a marker of catabolism (P = 0.03). In the nested case-control study, IGFBP-1 was increased after hypoglycemia, whereas the somatotropic axis and the counterregulatory hormones cortisol and glucagon did not change.ConclusionsDespite improved PICU outcome, IIT did not counteract the catabolic state of critical illness. Suppression of portal insulin may have resulted in lower bioavailable IGF-I.

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