The kinetic interactions among glucose, alanine, and urea metabolism were studied in both normal volunteers and in patients with sepsis by means of a primed, constant infusion of stable isotopes. In the normal volunteers, infusion of glucose at 4 mg/kg/min suppressed total glucose production, the rate of gluconeogenesis from alanine, and the production of urea, despite an increase in the rate of release and uptake of alanine. When the glucose infusion rate was increased to 8 mg/kg/min, the production of urea decreased further, even though gluconeogenesis from alanine was already suppressed by the first infusion. This additional N-sparing effect was explainable by an increase in glucose oxidation. In the patients with sepsis the basal rates of production of glucose and urea were elevated significantly. Glucose infusion (4 mg/kg/min) decreased hepatic glycogenolysis but not gluconeogenesis from alanine or urea production. At the glucose infusion rate of 8 mg/kg/min, glucose oxidation increased in the patients and urea production decreased. Thus in patients with sepsis a higher rate of glucose infusion is necessary to achieve nitrogen-sparing effects than is necessary in controls because of a lack of suppressibility of gluconeogenesis. Because of continued glucose production, during glucose infusion, hyperglycemia commonly develops during glucose infusion in sepsis. However, this effect does not necessarily indicate a complete inability of the patient with sepsis to benefit nutritionally from infused glucose, as we observed no decrement in the ability to oxidize infused glucose.
|Number of pages||12|
|State||Published - Jan 1 1985|