Nephron
Original Paper
Insulin Binding and Glycolytic Activity in Erythrocytes from Dialyzed and Nondialyzed Uremic PatientsWeisinger J.R. · Contreras N.E.I.R. · Cajias J. · Bellorin-Font E. · Amair P. · Gutierrez L. · Sylva V. · Paz-Martínez V.Centro Nacional de Diálisis y Trasplante, MSAS. Servicio de Nefrologia y Trasplante Renal, Hospital Universitario de Caracas, and Cátedra de Medicina I, Universidad Central de Venezuela, Caracas, Venezuela
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Article / Publication Details
Accepted: May 11, 1987
Published online: December 09, 2008
Issue release date: 1988
Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 0
ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)
For additional information: https://www.karger.com/NEF
Abstract
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.
© 1988 S. Karger AG, Basel
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Article / Publication Details
Accepted: May 11, 1987
Published online: December 09, 2008
Issue release date: 1988
Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 0
ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)
For additional information: https://www.karger.com/NEF
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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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