The relationship between precursor supply and hepatic glucose output (HGO) was examined in 8 control subjects and 12 trauma patients after a fasting period of approximately 60 hours. Glucose kinetics were measured with a primed-constant infusion of [U-14C]glucose and [6-3H]glucose. The basal rate of HGO was 5.45 +/- 0.22 micromol x kg-1 x min-1 in the controls and 13.16 +/- 0.76 micromol x kg-1 x min-1 following trauma (p < 0.001). Four hours after amino acid infusion of 1.3 g x kg-1 x 24 h-1, HGO in the controls was unchanged at 5.35 +/- 0.22 micromol x kg-1 x min-1 but it had decreased to 11.71 +/- 0.67 micromol x kg-1 after trauma (p < 0.001). We conclude that increasing the supply of gluconeogenic precursors does not stimulate HGO in normal subjects after fasting or after severe trauma and that factors other than to availability of amino acids are responsible for the enhanced rate of HGO in trauma patients.
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Long et al. (1996) studied this question.
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