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Research Article Free access | 10.1172/JCI113545

Nonbinding inhibitory antiinsulin receptor antibodies. A new type of autoantibodies in human diabetes.

G Boden, Y Fujita-Yamaguchi, R Shimoyama, J J Shelmet, L Tappy, I Rezvani, and O E Owen

Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

Find articles by Boden, G. in: PubMed | Google Scholar

Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

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Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

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Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

Find articles by Shelmet, J. in: PubMed | Google Scholar

Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

Find articles by Tappy, L. in: PubMed | Google Scholar

Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

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Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.

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Published June 1, 1988 - More info

Published in Volume 81, Issue 6 on June 1, 1988
J Clin Invest. 1988;81(6):1971–1978. https://doi.org/10.1172/JCI113545.
© 1988 The American Society for Clinical Investigation
Published June 1, 1988 - Version history
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Abstract

Sera and their IgG from 10/104 diabetic patients (five with insulin-dependent and five with noninsulin-dependent diabetes, NIDDM), contained antibodies that bound 125I-labeled purified human insulin receptors. 9 of these 10 sera failed to inhibit insulin binding (to rat hepatocytes and human placental membranes), did not stimulate glucose oxidation (by isolated rat adipocytes), and did not bind human placental IGF-1 receptors. Only one serum (and its IgG) modestly inhibited insulin binding and stimulated glucose oxidation. We conclude (a) that sera from 9/104 diabetics (five insulin-dependent and four noninsulin-dependent) contained a newly identified species of IgG antiinsulin receptor autoantibodies (AIRA), which bound to the insulin receptor at a locus different from the insulin binding site and did not inhibit insulin binding; and (b) that only 1/104 diabetic sera contained low-titer "conventional" antiinsulin receptor autoantibodies that bound to the insulin receptor at or near the insulin binding site, inhibited insulin binding and caused a clinical condition, which was difficult to distinguish from typical NIDDM.

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