ENDOGENOUS GLUCOSE-PRODUCTION FOLLOWING INJURY INCREASES WITH AGE

To evaluate the influence of aging on the increase in endogenous gluco se production that follows injury, are studied 22 fully resuscitated, clinically stable, previously healthy patients aged less than or equal to 30 yr or greater than or equal to 60 yr admitted to hospital follo wing injury, and 11 healthy volunteers in the same age groups. Endogen ous glucose production was determined using a primed constant infusion of D-glucose-6,6-(2)d(2). Urine cortisol and C-peptide were markedly higher in patients than volunteers (both P < 0.01), and urine C-peptid e was lower in older than in younger patients (P < 0.05). Urine cortis ol increased as a function of the interaction of age and Injury Severi ty Score (ISS) (r(2) = 0.40, P < 0.001). Intracellular water was marke dly lower and extracellular water greater in patients compared with vo lunteers (both P < 0.001), reflecting the loss of body cell mass and e xpansion of the extracellular space following injury. Endogenous gluco se production (milligrams per minute per liter intracellular water) wa s best described as a function of ISS and age-ISS interaction (r(2) = 0.35, all P < 0.05), and was increased 56% and 78% in younger and olde r patients, respectively, in comparison with the respective volunteer groups. Endogenous glucose production following injury increases in re lation to the severity of injury and patient age. Greater cortisol ela boration and diminished insulin secretion in older patients may contri bute to this age effect.