Measurement of the rates of basal pinocytosis of horseradish peroxidase and internalization of heat-aggregated IgG by macrophages from normal and streptozotocin-induced diabetic rats.

The rates of basal pinocytosis and internalization of Fc receptor-bound model immune complexes by macrophages from control (Group 1, n = 9), insulin-treated non-diabetic (2, n = 9), insulin-deficient diabetic (3, n = 8) and insulin-treated diabetic (4, n = 8) rats were measured. Pinocytic rates, as determined by uptake of horseradish peroxidase (HRP), were comparable for all experimental groups (1, 19.6 +/- 5.3; 2, 18.6 +/- 6.0; 3, 18.7 +/- 5.5; 4, 24.5 +/- 9.1; mean +/- 1 SD, pg per min per 10(6) cells, analysis of variance P greater than 0.05). The rates of internalization of Fc receptor-bound model immune complexes were decreased in insulin-treated non-diabetic rats (2, 41.7 +/- 10) and both groups of diabetic rats (3, 39 +/- 5.6; 4, 44.6 +/- 6.9) compared with control animals (1, 54.4 +/- 7.2; mean +/- 1 SD, percentage internalized per 10 min per 10(6) cells, analysis of variance P less than 0.01). Under the conditions of study, comparable amounts of model immune complexes were bound by macrophages from each of the groups; thus, the amount of internalized material was decreased in all three experimental groups (2, 3 and 4). These data suggest that insulin treatment, as well as the diabetic environment, can contribute to a decreased rate of internalization of Fc receptor-bound immune complexes, and may thereby contribute to impaired phagocytosis that has been demonstrated to occur in diabetes. These changes appear to be specific to Fc receptor-mediated internalization, as no differences in the rates of basal pinocytosis were observed.