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Endogenous Glucose Production Following Injury Increases with Age

Departments of Surgery and Physiology (J.M.W.), University of Ottawa; and Division of General Surgery and Loeb Institute for Medical Research (J.M.W., S.B.N., S.M.K.), Ottawa Civic Hospital, Ottawa, Canada

Address all correspondence and requests for reprints to: James M. Watters, Ottawa Civic Hospital, 1053 Carling Avenue, Ottawa, Ontario, Canada, K1Y 4E9.

To evaluate the influence of aging on the increase in endogenous glucose production that follows injury, we studied 22 fully resuscitated, clinically stable, previously healthy patients aged 30 yr or 60 yr admitted to hospital following injury, and 11 healthy volunteers in the same age groups. Endogenous glucose production was determined using a primed constant infusion of D-glucose-6,6-²d₂. Urine cortisol and C-peptide were markedly higher in patients than volunteers (both P < 0.01), and urine C-peptide was lower in older than in younger patients (P < 0.05). Urine cortisol increased as a function of the interaction of age and Injury Severity Score (ISS) (r² = 0.40, P < 0.001). Intracellular water was markedly lower and extracellular water greater in patients compared with volunteers (both P < 0.001), reflecting the loss of body cell mass and expansion of the extracellular space following injury. Endogenous glucose production (milligrams per minute per liter intracellular water) was best described as a function of ISS and age-ISS interaction (r² = 0.35, all P < 0.05), and was increased 56% and 78% in younger and older patients, respectively, in comparison with the respective volunteer groups. Endogenous glucose production following injury increases in relation to the severity of injury and patient age. Greater cortisol elaboration and diminished insulin secretion in older patients may contribute to this age effect.