Studies on insulin receptor in chronic renal failure

• Published in: Journal of Japanese Society for Dialysis Therapy Vol. 19; no. 2; pp. 183 - 197
• Main Author: Esaki, Kazuyoshi
• Format: Journal Article
• Language: Japanese
• Published: The Japanese Society for Dialysis Therapy 1986
• Subjects: 125I-insulin binding; average affinity; hemofiltration; insulin receptor; Scatchard analysis
• ISSN: 0911-5889; 1884-6211
• DOI: 10.4009/jsdt1985.19.183

This study was undertaken to analyze the deteriorated glucose tolerance in chronic renal failure and to investigate the effects of various blood purification methods on glucose tolerance by examining the results of intravenous glucose tolerance tests (ivGTT) and insulin binding ability to mature erythrocytes. Forty-two chronic renal failure patients, 11 undialyzed (UD), 22 hemodialyzed (HD) (10 acetate (HDA)-and 12 bicarbonate (HDB)-dialyzed) and 9 hemofiltrated (HF) patients, were chosen for this study. The UD patients showed deteriorated glucose tolerance, but both the HD and HF patients had improved glucose tolerance. 125I-insulin specific binding to erythrocytes from the UD patients was significantly lower than that for normal subjects, HD and HF patients. The HDA and HDB patients showed similar 125I-insulin specific binding to erythrocytes, which was significantly lower than that for normal subjects. However, there was no significant difference in the specific binding value between HF and normal subjects. From De Meyts analyses of the Scatchard plots, the unoccupied receptor site affinity constant, Ke, was determined to be as follows: normal subiects, 0.437×108M-1; UD, 0.650×108M-1; HD, 0.490×108M-1; HF, 0.345×108M-1. The numbers of insulin receptor sites per erythrocyte were as follows: normal subjects, 450; UD, 205; HD, 380; HF, 590. These results suggested that a decrease in the number of insulin receptor sites was responsible for the deteriorated glucose tolerance in chronic renal failure. Although the insulin-binding ability was impaired in HD patients, glucose tolerance was improved, which might be explained by compensation at the expense of insulin oversecretion. In HF patients, the insulin-binding ability was found to be normal, probably due to the increase in the number of insulin receptor sites. Therefore, HF may be a better blood purification method than HD for improving glucose tolerance in chronic renal failure.