Serum insulin concentrations were measured serially in seven nondiabetic subjects following a rapid intravenous glucose load during a preinfection control period, during early clinical respiratory tularemia, and again in convalescence following therapy. Within twenty-four hours of onset of clinical illness the rate of glucose disappearance from the blood had diminished significantly (p<0.05). At the same time there was a brisk rise in insulin levels reaching higher peak concentrations and falling more slowly than the response observed during the preinfection control period. The pattern during clinical illness was different from that described after intravenous glucose loading in maturity onset diabetes or obesity and may have been influenced by glucocorticoid excess. Increased whole blood pyruvate concentrations following glucose loading during clinical illness were compatible with heightened glucocorticoid ction. The magnitude of insulin clinical illness was significantly increased (p<0.02) and was directly related to height of fever In contrast, the rate of glucose disappearance was inversely related to fever. The inverse relationship of the magnitude of insulin output to the rate of glucose reappearance suggested a peripheral inhibition of insulin action during infection. Although fever may have played a role during acute illness, the persistence of an abnormal insulin response in one patient during convalescence suggested that this change was not dependent upon fever alone. Other factors that may have contributed to the peripheral inhibition of insulin action during clinical illness are briefly discussed.

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