Adjuvant recombinant human growth hormone does not augment endogenous glucose production in total parenteral nutrition-fed multiple trauma patients

Hyperglycemia and insulin resistance are well-known, consistent responses to severe injury. The purpose of this study was to investigate the mechanism for the further exaggerated hyperglycemia due to adjuvant recombinant human growth hormone (rhGH) treatment in multiple trauma patients. We have measured in 20 adult severely injured, highly catabolic, hypermetabolic, multiple trauma patients, the glucose kinetics (appearance, clearance, oxidation, and recycling) once in the basal state (study I), 48 to 60 hours after injury but before starting nutritional therapy, and again (study II) after 7 days of intravenous nutrition (1.1 times resting energy expenditure, 250 mg nitrogen [N]/kg/d) with or without adjuvant rhGH. Group H (n = 10) randomly received daily (8 AM) rhGH (0.15 mg/kg/d) and group C (n = 10) received the vehicle of infusion. Adjuvant rhGH treatment in intravenously fed trauma patients (1) increases plasma insulin-like growth factor-1 (IGF-1) and insulin concentrations, (2) improves N balance, and (3) exaggerates the hyperglycemic response without affecting endogenous glucose output, glucose oxidation, or recycling. The mechanism for the hyperglycemic hyperinsulinemia in trauma may be due to a defective nonoxidative glucose disposal, as well as inhibition of glucose transport activity into tissue cells.