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      Insulin-Like Growth Factor (IGF)-I, IGF Binding Protein (IGFBP)-3, Phosphoisoforms of IGFBP-1 and Postnatal Growth in Very-Low-Birth-Weight Infants

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          Abstract

          Small preterm infants experience a unique postnatal period characterized by slow growth, inadequate nutrition and growth inhibiting treatments. Many have already been growth-restricted in utero. Studying this period is important when developing growth optimizing strategies for these infants and, in a broader context, as a model of extreme conditions that restrict growth. By following short-term growth of 48 very-low-birth-weight (VLBW; birth weight <1,500 g) infants for 9 postnatal weeks, we found that circulating insulin-like growth factor (IGF)-I and IGF binding protein (IGFBP)-3 levels are low and reflect rigorously measured (knemometry and weight) concurrent growth velocity. Moreover, weight growth velocity is correlated with the ratio of lesser to highly phosphorylated IGFBP-1 but not with absolute IGFBP-1 concentrations. Thus, IGF-I, IGFBP-3 and the phosphorylation status of IGFBP-1 in circulation are likely to be involved in growth regulation during the postnatal period in VLBW infants.

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          Most cited references 16

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          Normal growth and development in the absence of hepatic insulin-like growth factor I.

          The somatomedin hypothesis proposed that insulin-like growth factor I (IGF-I) was a hepatically derived circulating mediator of growth hormone and is a crucial factor for postnatal growth and development. To reassess this hypothesis, we have used the Cre/loxP recombination system to delete the igf1 gene exclusively in the liver. igf1 gene deletion in the liver abrogated expression of igf1 mRNA and caused a dramatic reduction in circulating IGF-I levels. However, growth as determined by body weight, body length, and femoral length did not differ from wild-type littermates. Although our model proves that hepatic IGF-I is indeed the major contributor to circulating IGF-I levels in mice it challenges the concept that circulating IGF-I is crucial for normal postnatal growth. Rather, our model provides direct evidence for the importance of the autocrine/paracrine role of IGF-I.
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            Intrauterine growth retardation and postnatal growth failure associated with deletion of the insulin-like growth factor I gene.

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              Circulating concentrations of insulin-like growth factor-I and development of glucose intolerance: a prospective observational study.

              Results of experimental and clinical studies suggest that insulin-like growth factor-I (IGF-I) and IGF binding protein-1 (IGFBP-1) could be important determinants of glucose homoeostasis. However, experimental models might also reflect compensatory and adaptive metabolic processes. We therefore prospectively examined the associations between circulating concentrations of IGF-I and IGFBP-1 and development of glucose tolerance. Participants in this cohort study were a random sample of 615 normoglycaemic men and women aged 45-65 years. Participants underwent oral glucose tolerance testing based on WHO definitions and criteria in 1990-92 and 1994-96. At the baseline visit, we measured serum concentrations of IGF-I and IGFBP-1, and assessed the relation between these peptides and subsequent glucose intolerance. At 4.5 years of follow-up, 51 (8%) of 615 participants developed impaired glucose tolerance or type-2 diabetes. After adjustment for correlates of IGF-I and risk factors for glucose intolerance, the odds ratio for risk of impaired glucose tolerance or type-2 diabetes for participants with IGF-I concentrations above the median (> or = 152 microg/L) compared with those with concentrations below the median (<152 microg/L) was 0.50 (0.26-0.95). Consistent with this finding, IGF-I also showed a significant inverse association with subsequent 2-h glucose concentrations, which was independent of correlates of IGF-I and risk factors for glucose tolerance (p for linear trend=0.026). We also found that this inverse association was independently modified by IGFBP-1 (p for interaction=0.011). These data show that circulating IGF-I and its interaction with IGFBP-1 could be important determinants of glucose homoeostasis and provide further evidence for the possible protective role of IGF-I against development of glucose intolerance.
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                Author and article information

                Journal
                HRE
                Horm Res Paediatr
                10.1159/issn.1663-2818
                Hormone Research in Paediatrics
                S. Karger AG
                978-3-8055-7687-1
                978-3-318-01053-4
                1663-2818
                1663-2826
                2003
                December 2003
                17 November 2004
                : 60
                : Suppl 3
                : 124-130
                Affiliations
                Helsinki University Central Hospital, Hospital for Children and Adolescents, Helsinki, Finland
                Article
                74513 Horm Res 2003;60(suppl 3):124–130
                10.1159/000074513
                14671409
                © 2003 S. Karger AG, Basel

                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. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, References: 39, Pages: 7
                Categories
                SGA Satellite Symposium

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