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Original Articles

Antibodies to Insulin-Like Growth Factor I Receptors in Diabetes and Other Disorders

  1. Luc Tappy,
  2. Yoko Fujita-Yamaguchi,
  3. Thomas R LeBon and
  4. Guenther Boden
  1. Department of Medicine, Division of Metabolism/Endocrinology, General Clinical Research Center, Temple University School of Medicine Philadelphia, Pennsylvania the Department of Molecular Genetics, Beckman Research Institute of the City of Hope Duarte, California
  1. Address correspondence to Guenther Boden, MD, Temple University Health Sciences Center, 3401 North Broad Street, Philadelphia, PA 19140.
Diabetes 1988 Dec; 37(12): 1708-1714. https://doi.org/10.2337/diab.37.12.1708
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Abstract

A newly developed immunoprecipitation assay, with 125I-labeled highly purified human placental insulin-like growth factor I (IGF-I) receptor, was used to search for IGF-I-receptor antibodies in human sera. Eleven of 141 patient sera tested (7.8%) immunoprecipitated labeled IGF-I receptor. Immunoprecipitation was comparable with sera and IgG prepared from these sera. Seven of the 11 sera (3 of 31 with rheumatic disorders, 3 of 48 with non-insulin-dependent diabetes, and 1 of 52 with insulin-dependent diabetes) failed to inhibit IGF-I binding to human placental membranes and thus contained non-binding-inhibitory IGF-I-receptor antibodies. Their pathophysiological function remained uncertain. The remaining 4 sera (2 of 3 with type B severe insulin resistance, 1 of 7 with polycystic ovary syndrome (PCO), and 1 of 31 with rheumatic disorders) inhibited IGF-I binding. Plasma IGF-I concentrations were elevated (663 and 802 ng/ml, respectively) in 2 patients (1 with PCO and another with systemic lupus erythematosus) with binding-inhibitory IGF-I-receptor antibodies, suggesting IGF-I resistance that was probably mediated by the IGF-I-receptor antibodies. In conclusion, we identified two species of human IGF-I-receptor antibodies. Sera from 7 of 141 patients tested contained IgG autoantibodies that bound to the IGF-I receptor at a locus different from the IGF-I binding site and did not inhibit IGF-I binding. Sera from 4 of 141 patients contained antibodies that bound to the IGF-I receptor at or near the IGF-I binding site, inhibited IGF-I binding, and probably caused IGF-I resistance.

  • Received October 20, 1987.
  • Revision received June 30, 1988.
  • Accepted June 30, 1988.
  • Copyright © 1988 by the American Diabetes Association

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December 1988, 37(12)
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Antibodies to Insulin-Like Growth Factor I Receptors in Diabetes and Other Disorders
Luc Tappy, Yoko Fujita-Yamaguchi, Thomas R LeBon, Guenther Boden
Diabetes Dec 1988, 37 (12) 1708-1714; DOI: 10.2337/diab.37.12.1708

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Antibodies to Insulin-Like Growth Factor I Receptors in Diabetes and Other Disorders
Luc Tappy, Yoko Fujita-Yamaguchi, Thomas R LeBon, Guenther Boden
Diabetes Dec 1988, 37 (12) 1708-1714; DOI: 10.2337/diab.37.12.1708
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