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OLUF PEDERSEN, HENNING BECK-NIELSEN, NIELS SCHWARTZ SØRENSEN, ARNE SVEJGAARD, Heterogeneity of Insulin Receptors in Patients with Untreated Insulin-Dependent Diabetes Mellitus, The Journal of Clinical Endocrinology & Metabolism, Volume 55, Issue 1, 1 July 1982, Pages 30–39, https://doi.org/10.1210/jcem-55-1-30
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Abstract
[125I]Insulin binding to monocytes (36 diabetics) and erythrocytes (11 diabetics) from newly discovered insulindependent diabetics was measured before treatment and during the first 6 months of insulin and diet therapy. At the onset of diabetes, the tracer [125I]insulin binding to monocytes showed great heterogeneity, with the distribution of binding values being significantly different from that of healthy controls (P<0.01). In an attempt to examine if the insulin receptor reactivity at the onset of insulin-dependent diabetes might be genetically controlled, complete HLA-ABC and HLA-DR typings were performed. However, no significant relationships were detected between monocyte insulin binding and HLA antigens. The longitudinal studies showed that the patients who initially had higher monocyte insulin binding than the mean of healthy controls (high binders) exhibited a significant decrease in insulin binding during 10 days of treatment, whereas those with initially decreased monocyte insulin binding (low binders) showed a significant increase in insulin binding after 10 days. In both groups, insulin binding to monocytes was normal after 6 months. When monocyte insulin binding data were analyzed in relation to the hormonal-metabolic status on the debut of diabetes, it was found that the patients with initially increased insulin binding to monocytes had plasma insulin concentrations close to zero, and they were extremely ketotic. Their raised cellular insulin binding, therefore, might be secondary to the severe insulin deficiency and hyperketonemia. Although low binders, on the average, had significantly higher plasma insulin concentrations and significantly lower plasma concentrations of ketone bodies than did high binders, they were definitely insulin deficient and ketotic. The apparent failure of an insulin receptor upregulation in these patients might be due to an effect of prolonged acidosis in the presence of a less pronounced hyperketonemia. Insulin binding to erythrocytes at the onset of diabetes and during treatment for the first 10 days showed a pattern similar to that of insulin binding to monocytes. However, at variance with the changes in monocyte insulin binding, the erythrocyte insulin binding values after treatment for 6 months were significantly increased compared to binding values at the onset of diabetes and binding values in normals. The increased erythrocyte insulin binding may be due to a concomitant increase in the mean erythrocyte volume.
