1. The work utilized a model of uncomplicated abdominal surgery (laparotomy under ether anaesthesia) to delineate the effects of abdominal trauma on glucose homoeostasis in the fed rat.
2. Regulation of glucose production and utilization was investigated by observing the response to the administration of glucose, insulin plus glucose and 5-methylpyrazole 3-carboxylic acid.
3. Glucose administration suppressed hepatic glucose output as assessed by portal–venous concentration differences in control or surgically stressed rats. In contrast, glycaemia was increased and lactaemia decreased in the latter group. Portal–venous concentrations differences for lactate were unaffected.
4. Surgery increased plasma fatty acid concentrations and the antilipolytic response to glucose or glucose plus insulin was diminished. Post-operative increases in fatty acid concentrations were associated with inhibition of hepatic pyruvate dehydrogenase complex which was reversed by insulin, indicating a differential sensitivity of adipose tissue and liver to the hormone.
5. The model of surgical stress utilized, while affecting extrahepatic glucose disposal, did not elicit depletion of liver glycogen or inactivation of l-pyruvate kinase.
6. It is concluded that the initial response to uncomplicated abdominal surgery involves carbohydrate conservation rather than increased glucose production, with effects to decrease extrahepatic glucose uptake and hepatic glucose oxidation.