To investigate the mechanism of the reported abnormality of polymorphonuclear leukocyte (neutrophil) function in diabetes, the burst of oxidative activity accompanying the killing reaction and the neutrophil iodination reaction were measured in 21 stable, insulintreated diabetic subjects and 32 nondiabetic subjects of similar age range. Responses to standard killed preparations of Candida albicans (C. albicans) (glucose oxidation and neutrophil iodination) and Staphylococcus aureus (S. aureus) (neutrophil iodination) were studied. The iodination reaction was studied using the subjects' neutrophils suspended both in autologous serum and in pooled normal human serum, and the glucose oxidation test was performed using the neutrophils in pooled normal human serum.
There was a significant decrease in the conversion of 14C-1-glucose to 14CO2 in the neutrophils from diabetics [0.47 ± 0.04 (SE) cf. 0.64 ± 0.04 nmol/2 × 106 neutrophils/60 min, P < 0.005] and in neutrophil iodination in response to S. aureus in both autologous serum (diabetics .089 ± 0.008 cf. 0.114 ± 0.008 nmol iodine/106 neutrophils/90 min, P < 0.025) and in pooled human serum (diabetics 0.086 ± 0.009 cf. 0.105 ± 0.006, P < 0.05). There was no significant difference in neutrophil iodination in response to C. albicans. There was a significant negative correlation between the diabetics' fasting plasma glucose level and neutrophil iodination in response to S. aureus in pooled human serum (r = - 0.54, P < 0.05), but not between fasting plasma glucose and glucose oxidation.
It is concluded that there are significant decreases in stimulated glucose oxidation and in the neutrophil iodination reaction (reflecting decreased function of the myeloperoxidase-hydrogen peroxide-halide microbicidal system) in neutrophils from insulin-treated dia-betic subjects. These abnormalities may contribute to the defective bactericidal activity of diabetic neutrophils.