Erythrocyte Insulin Receptors in Chronic Renal Failure

Gambhir, Kanwal K.; Archer, J. A.; Nerurkar, Shriniwas G.; Cruz, Iluminado A.; Sanders, Michael

doi:10.1159/000182086

Cited by 22 publications

(8 citation statements)

References 29 publications

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“…The decreased maximum bindings were due to the reduction of receptor concentration, but not the alterations of binding affinity of receptors. Our findings in uremic children coincided well with that of adults reported by Gambhir et al (1981). In their paper, the maximum binding in dialyzed patients and the average affinity in uremic patients were significantly elevated, whereas in our patients these parameters were not different from that of control.…”

Section: Discussionsupporting

confidence: 92%

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Insulin Receptor of Erythrocytes and Glucose Metabolism in Uremic Children

Namikawa¹,

Fujimoto²,

Furuse³

et al. 1983

Horm Metab Res

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This study represents the results of oral glucose tolerance test (O-GTT) of 28 children with chronic renal failure, including 12 undialyzed and 16 dialyzed cases, compared to their own insulin receptors of erythrocytes. 7 of the 12 undialyzed patients (58.3%) represented abnormal O-GTT, while in dialyzed patients 3 of 16 cases (18.8%) had abnormal O-GTT. The maximum binding of 125 l-insulin to erythrocytes, 6.34 ± 1.93% in dialyzed patients, was significantly lower (p < 0.05) than 7.73 ± 1.03% in controls, and 4.87 ± 1.01% in undialyzed patients was significantly lower than both dialyzed (p < 0.05) and controls (p < 0.001). In undialyzed patients, 350 ± 221 binding sites/cell of insulin receptor was significantly fewer than 544 ± 207 binding sites/cell in controls (p < 0.05), but no significance was detected when compared to the 562 ± 331 binding sites/cell in dialyzed patients, because of the large variation in dialyzed patients. The average affinity of empty site (Ke x 10 7 /M) that 4.18 ± 2.73 in undialyzed patients, 3.40 ± 2.32 in dialyzed patients and 3.37 ± 1.05 in controls, had no significance between any two of the three. There were no significant correlations between receptor concentration and the sum of blood sugar (DBS) or the sum of insulin (SIRI), and no correlation between receptor concentration and BUN or creatinine. Furthermore, no significant relationships could be found when comparing BUN or creatinine with O-GTT. However, if the patients were divided into groups as normal and abnormal of O-GTT, significantly higher values of SBS (p < 0.001) and lower concentrations of insulin receptor (p < 0.05) were found in the abnormal group. No difference was found in SIRI and Ke. In addition, a significantly lower value of serum calcium concentration was found in the abnormal group of O-GTT.

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Section: Discussionsupporting

confidence: 92%

“…Recently, Gambhir et al (Gambhir, Archer, Received: 4 Apr. 1982 Accepted: 25 July 1982 Nerurkar, Cruz and Sanders 1981;Gambhir, Nerurkar, Cruz and Hosten 1980) demonstrated the decreased receptor concentration of insulin in erythrocytes from adult uremic patients.…”

Section: Introductionmentioning

confidence: 99%

Insulin Receptor of Erythrocytes and Glucose Metabolism in Uremic Children

Namikawa¹,

Fujimoto²,

Furuse³

et al. 1983

Horm Metab Res

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“…Gambhir et al [13] studied insulin binding to human erythrocytes in uremic patients and found de creased specific insulin binding in undialysed uremics and increased binding in dialysed patients. In a previous paper [1], we provided evidence that the improvement in insulin sensitivity after dialysis could be at least partly due to cor rection of the binding defect.…”

Section: Discussionmentioning

confidence: 99%

“…Decreased sensitivity of peripheral tissues to insulin can be caused by a defect in binding of insulin to its re ceptors, by postreceptor defect, or both. Recently, we [1] and others [13] reported on decreased insulin binding to erythrocytes from uremic patients. We demonstrated that a defect in insulin binding could be reversed by hemo dialysis to an extent predicted by efficiency of elimination of uremic waste products [1].…”

Section: Introductionmentioning

confidence: 88%

Inhibitor of Insulin Binding to Erythrocytes in Plasma of Uremic Patients

Milutinović¹,

Breyer

Janković³

et al. 1983

Nephron

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Previously, we have shown that insulin binding (IB) to erythrocytes was decreased in uremic patients and that hemodialysis corrected the receptor defect. In the present study cross-incubation experiments were performed using uremic and control erythrocytes and plasma. Incubation of control erythrocytes with uremic plasma resulted in a 60% decrease in specific insulin binding, and progressive dilutions of uremic plasma revealed a parallel decrease in degree of inhibition suggesting the presence of an inhibitor of insulin binding in uremic plasma. Plasma obtained from uremic patients exhibiting lower IB to their erythrocytes was more potent in inhibition of IB to control erythrocytes, i.e. predialysis in comparison with postdialysis plasma. The alteration of IB was reversible since incubation of uremic erythrocytes with normal plasma restored IB towards normal values. Subjects having higher IB to their erythrocytes had more efficient plasma in restoring IB to uremic erythrocytes. The data indicate that alteration of insulin binding in uremia is mediated by dialysable plasma inhibitors. The possibility that humoral factors affecting binding of insulin to its receptors can in this way influence the sensitivity of peripheral tissues to insulin is considered.

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“…Studies from several laboratories have yielded conflicting results regarding insulin binding to cells from uremic individu als. Several studies have reported normal insulin binding to cells from uremic patients [3][4][5][6] or from uremic rats [7,8], Others, however, have reported decreased insulin binding to cells from uremic [9][10][11] or dialysis patients [6].…”

Section: Introductionmentioning

confidence: 99%

Insulin Binding and Glycolytic Activity in Erythrocytes from Dialyzed and Nondialyzed Uremic Patients

Weisinger¹,

Contreras²,

Cajias³

et al. 1988

Nephron

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Insulin resistance in uremia has been attributed to impaired hormone-receptor binding or to postbinding defects. Oral glucose tolerance tests, insulin binding, and in vitro glycolytic activity were studied in purified red blood cells from normal control subjects (C) and from uremic patients belonging to three groups: nondialyzed (U), on chronic hemodialysis (HD), and on continuous ambulatory peritoneal dialysis (CAPD). Glucose intolerance and hyperinsulinemia were demonstrated in all groups of patients. Maximal specific binding of ¹²⁵I-insulin to erythrocytes, kinetically derived receptor numbers per cell, and affinity constants for insulin binding did not differ between control and patient groups. No correlation was found between the degree of glucose intolerance and insulin binding parameters. Basal lactate production by erythrocytes incubated invitro was significantly higher in U and HD patients than in Cwhereas CAPD patients did not differ from C in this respect. Addition of 1 mI dibutiryl-cAMP and 0.5 mM isobutyl-methyl-xanthine during incubation of erythrocytes caused an increase in the rate of lactate production that was similar in magnitude in the U, HD and C groups, whereas cells from CAPD subjects showed a significantly larger absolute response to these compounds after 1 h of incubation. There was no evidence of impairment of glycolytic capacity in red blood cells from uremic patients. In addition, no correlation was found between the degree of glucose intolerance and basal or stimulated lactate production by erythrocytes. Our results obtained in human erythrocytes suggest that the insulin resistance observed in uremia does not involve a defect in hormone binding or in the intracellular capacity to utilize glucose through glycolysis.

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Erythrocyte Insulin Receptors in Chronic Renal Failure

Cited by 22 publications

References 29 publications

Insulin Receptor of Erythrocytes and Glucose Metabolism in Uremic Children

Insulin Receptor of Erythrocytes and Glucose Metabolism in Uremic Children

Inhibitor of Insulin Binding to Erythrocytes in Plasma of Uremic Patients

Insulin Binding and Glycolytic Activity in Erythrocytes from Dialyzed and Nondialyzed Uremic Patients

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