1. In
sepsis various processes of carbohydrate metabolism, such as hepatic gluconeogenesis and glycolysis, are altered.
Phosphofructokinase-1, a key glycolytic
enzyme, is controlled in the long term via regulation of synthesis and degradation of the
protein itself, while in the short term it is regulated by allosteric effectors, such as
fructose 2,6-bisphosphate (the most potent). In the present study hepatic
phosphofructokinase-1 activity as well as
phosphofructokinase-2 activity and the concentration of
fructose 2,6-bisphosphate were assayed to determine if they might contribute to the derangement of carbohydrate metabolism seen commonly in
sepsis. 2. The levels of
glycogen and
fructose 2,6-bisphosphate and the activity of
phosphofructokinase-1 and
phosphofructokinase-2 were determined in hepatic biopsies obtained at
laparotomy from six patients with and seven patients without abdominal septic foci. 3. A significant increase in plasma
lactate concentration was observed in the septic patients, whereas no significant differences in tissue
glycogen content or plasma
glucose concentration were seen between the groups. 4. No significant change in plasma
insulin concentration was observed. However, levels of the counter-regulatory
hormones (
glucagon,
cortisol and
adrenaline) were elevated in the septic patients. 5. A 60% decrease in hepatic
phosphofructokinase-1 activity was seen in the septic patients. However, no significant changes in hepatic
phosphofructokinase-2 activity and
fructose 2,6-bisphosphate content were observed in the septic patients. 6. The present results demonstrate that the decrease in hepatic
phosphofructokinase-1 activity occurring in
sepsis does not appear to reflect alterations in the concentration of
fructose 2,6-bisphosphate.