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Vol. 62, Suppl. 1, 2004
Issue release date: February 2005
Section title: Efficacy
Horm Res 2004;62(suppl 1):77–82
(DOI:10.1159/000080763)

Role of Insulin-Like Growth Factor Iin Maintaining Normal Glucose Homeostasis

Clemmons D.R.
Department of Medicine, UNC School of Medicine, Chapel Hill, N.C., USA

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Article / Publication Details

First-Page Preview
Abstract of Efficacy

Published online: 3/10/2005

Number of Print Pages: 6
Number of Figures: 3
Number of Tables: 0

ISSN: 1663-2818 (Print)
eISSN: 1663-2826 (Online)

For additional information: http://www.karger.com/HRP

Abstract

Insulin-like growth factor I (IGF-I) has significant structural homology with insulin. IGF-I has been shown to bind to insulin receptors to stimulate glucose transport in fat and muscle, to inhibit hepatic glucose output and to lower blood glucose while simultaneously suppressing insulin secretion. However, the precise role of IGF-I in maintaining normal glucose homeostasis and insulin sensitivity is not well defined. Studies in patients with diabetes have shown that in insulin-deficient states, serum IGF-I concentrations are low and increase with insulin therapy. Similarly, administration of insulin via the portal vein results in optimization of plasma IGF-I concentrations. A patient with an IGF1 gene deletion was shown to have severe insulin resistance that improved with IGF-I therapy. Studies conducted in experimental animals have shown that if IGF-I synthesis by the liver is deleted, the animals become insulin-resistant, and this is improved when IGF-I is administered. Likewise, deletion of the IGF-I receptor in muscle in mice induces severe insulin resistance. Administration of IGF-I to patients with type 2 diabetes mellitus has been shown to result in an improvement in insulin sensitivity and a reduction in the requirement for exogenously administered insulin to maintain glucose homeostasis. A polymorphism in the IGF1 gene that has been shown to reduce serum IGF-I results in an increased prevalence of type 2 diabetes. Taken together, these findings support the conclusion that IGF-I is necessary for normal insulin sensitivity, and impairment of IGF-I synthesis results in a worsening state of insulin resistance.


  

Author Contacts

Dr. D.R. Clemmons
CB 7170 Endocrinology
UNC School of Medicine
Chapel Hill, NC 27599 (USA)
Tel. +1 919 966 4735, Fax +1 919 966 6025, E-Mail endo@med.unc.edu

  

Article Information

Number of Print Pages : 6
Number of Figures : 3, Number of Tables : 0, Number of References : 18

  

Publication Details

Hormone Research (From Development Endocrinology to Clinical Research)

Vol. 62, No. Suppl. 1, Year 2004 (Cover Date: Released February 2005)

Journal Editor: P. Czernichow, Paris
ISSN: 0301–0163 (print), 1423–0046 (Online)

For additional information: http://www.karger.com/hre


Article / Publication Details

First-Page Preview
Abstract of Efficacy

Published online: 3/10/2005

Number of Print Pages: 6
Number of Figures: 3
Number of Tables: 0

ISSN: 1663-2818 (Print)
eISSN: 1663-2826 (Online)

For additional information: http://www.karger.com/HRP


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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 goverment 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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