Insulin receptors on monocytes from patients with ketosis-prone diabetes mellitus.

Abstract

I-125-Insulin binding to its receptor on monocytes was measured in 30 young, insulin-treated diabetic outpatients and in 13 newly diagnosed, ketotic diabetic patients before and after insulin treatment. In insulin-treated diabetic outpatients, insulin binding was similar on average to that of 25 age-matched normal subjects. A slight but statistically significant negative relationship was found between the insulin concentration required to displace specific binding of I-125-insulin by 50 per cent and the plasma concentration of ketone bodies (R = −0.46, p < 0.02), indicating a positive correlation between apparent receptor affinity and the plasma concentration of ketone bodies. No correlation was found between insulin binding and total plasma insulin concentration. Insulin binding to monocytes from newly diagnosed diabetic patients exhibited large variability. Based on the initial insulin binding values and the receptor response to insulin treatment, the patients could be divided into two groups. Group 1 comprised eight diabetic subjects who had had specific cell-binding fractions at an insulin tracer concentration above the median of normal subjects before therapy; after insulin treatment for 10 days, insulin binding was restored to normal. Group 2 consisted of five diabetic patients who had had specific cell-binding fractions at a tracer level below the median of normal subjects when admitted; insulin therapy caused no significant change in insulin binding. In both groups of newly diagnosed, diabetic patients, no correlation could be found between the cellular insulin binding and the plasma concentrations of insulin and ketone bodies. We conclude that (1) insulin-treated diabetic outpatients have normal insulin binding to monocytes; (2) among newly diagnosed, ketotic diabetics with identical metabolic presentation, some may have a raised but reversible insulin binding initially, while others seem to have defective cellular insulin binding in addition to insulin deficiency; and (3) no consistent relationships exist between the plasma levels of insulin and ketone bodies and the insulin binding on monocytes from insulin-dependent diabetics.