Glucose Tolerance, Insulin Release, and Insulin Binding to Monocytes in Kidney Transplant Recipients

In order to evaluate glucose tolerance following renal transplantation, intravenous glucose tolerance tests (IVGTT), with evaluation of hormonal responses to the intravenous glucose load and percent specific 125I-insulin binding to peripheral blood monocytes, were studied in eight clinically stable...

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Veröffentlicht in:Am J Kidney Dis; (United States) 1982-03, Vol.1 (5), p.302-308
Hauptverfasser: Briggs, William A., Wielechowski, Kenn S., Mahajan, Sudesh K., Migdal, Stephen D., McDonald, Franklin D.
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Sprache:eng
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Zusammenfassung:In order to evaluate glucose tolerance following renal transplantation, intravenous glucose tolerance tests (IVGTT), with evaluation of hormonal responses to the intravenous glucose load and percent specific 125I-insulin binding to peripheral blood monocytes, were studied in eight clinically stable kidney transplant recipients. For comparison purposes, identical studies were done in eight control subjects and seven clinically stable hemodialysis patients. One transplant recipient was glucose intolerant, with fasting hyperglycemia, elevated HbA1c, and abnormal glucose decay constant. Impaired pancreatic insulin release appeared to be the major factor accounting for his glucose intolerance. The seven glucose-tolerant transplant recipients had significantly increased insulin release during IVGTT compared to control subjects, and significant correlations were found among insulin release, glucose decay constant, and fasting blood sugar in those patients. Insulin binding to monocytes was significantly greater in transplant recipients than control subjects due to an increase in insulin binding capacity per cell. A significant correlation was found between percent specific 125I-insulin binding and steroid dose, expressed as mg/kg body weight/day, in those patients. Thus, chronic steroid administration does not cause glucose intolerance in transplant recipients who manifest steroid-associated increases in pancreatic insulin release and cellular insulin binding capacity.
ISSN:0272-6386
1523-6838
DOI:10.1016/S0272-6386(82)80030-9