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      Insulin-Like Growth Factor -I Deficiency


      Hormone Research in Paediatrics

      S. Karger AG

      Growth, Growth hormone, IGF-I system, IGF-I, GHI, Insulin insensitivity

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          The insulin-like growth factor (IGF) system composed of two ligands, their receptors and regulatory proteins (acid-labile subunit and IGF-binding proteins) plays a central role in the regulation of growth and development in mammals. In addition to its key role in the stimulation of cellular proliferation and growth, IGF-I has important effects on carbohydrate, protein and bone metabolism. The molecular biology and physiology of the IGF system are complex, resulting in many potential mechanisms of IGF deficiency. Briefly, IGF-I deficiency may result from a primary defect in the IGF-I gene, its promoters, or may be secondary to a defect outside the gene itself. It may also result as a consequence of growth hormone (GH) deficiency, GH receptor/post-receptor abnormalities or abnormalities of the IGF-I receptor. The purpose of this presentation is to review the different types of IGF-I deficiency using the well-characterized clinical conditions with its associated biochemical and molecular defects. The clinical consequences in terms of phenotype-genotype, linear growth and body composition in patients with primary and secondary IGF deficiency will be presented, together with results from recombinant human (rh)IGF-I replacement therapy. Finally, as primary IGF-I deficiency is associated with insulin resistance, some of the metabolic actions of IGF-I will be briefly discussed.

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          Author and article information

          Horm Res Paediatr
          Hormone Research in Paediatrics
          S. Karger AG
          17 November 2004
          : 55
          : Suppl 1
          : 17-20
          Paediatric Endocrinology Section, Department of Endocrinology, St. Bartholomew’s Hospital, London, UK
          63457 Horm Res 2001;55(suppl 1):17–20
          © 2001 S. Karger AG, Basel

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          Page count
          Tables: 1, References: 19, Pages: 4


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