Metabolism - Clinical and Experimental
Volume 44, Supplement 4 , Pages 50-57, October 1995

Nutritional regulation of insulin-like growth factor-I☆

  • Jean-Marie Ketelslegers

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Jean-Marie Ketelslegers, MD, PhD, Unité de Diabétologie et Nutrition, Université Catholique de Louvain, Tour Claude Bernard, UCL15474, Avenue Hippocrate 54, B-1200 Bruxelles, Belgium.
    • Unit of Diabetes and Nutrition, Department of Internal Medicine, School of Medicine, Catholic University of Louvain, Brussels, Belgium
    • Department of Pediatrics, School of Medicine, University of North Carolina, Chapel Hill, NC, USA
    • ,
  • Dominique Maiter

      Affiliations

    • Unit of Diabetes and Nutrition, Department of Internal Medicine, School of Medicine, Catholic University of Louvain, Brussels, Belgium
    • Department of Pediatrics, School of Medicine, University of North Carolina, Chapel Hill, NC, USA
    • ,
  • Marc Maes

      Affiliations

    • Unit of Diabetes and Nutrition, Department of Internal Medicine, School of Medicine, Catholic University of Louvain, Brussels, Belgium
    • Department of Pediatrics, School of Medicine, University of North Carolina, Chapel Hill, NC, USA
    • ,
  • Louis E. Underwood

      Affiliations

    • Unit of Diabetes and Nutrition, Department of Internal Medicine, School of Medicine, Catholic University of Louvain, Brussels, Belgium
    • Department of Pediatrics, School of Medicine, University of North Carolina, Chapel Hill, NC, USA
    • ,
  • Jean-Paul Thissen

      Affiliations

    • Unit of Diabetes and Nutrition, Department of Internal Medicine, School of Medicine, Catholic University of Louvain, Brussels, Belgium
    • Department of Pediatrics, School of Medicine, University of North Carolina, Chapel Hill, NC, USA

Abstract 

Several lines of evidence indicate that in the human, insulin-like growth factor-I (IGF-I) is nutritionally regulated. Both energy and protein availability are required for maintenance of IGF-I. Measurements of serum IGF-I constitute a sensitive means for monitoring the response of acutely ill patients to nutritional intervention. Serum IGF-I may also serve as a marker for evaluation of nutritional status. Our findings and those of others in animal models suggest that nutrients influence synthesis and action of IGF-I and its binding proteins (IGFBPs) at multiple levels. In fasting, liver growth hormone (GH) binding is decreased, providing one explanation for decreased IGF-I. In protein restriction, GH receptors are maintained, but there is evidence for a postreceptor defects. The latter results from pretranslational and translational defects. Amino acid availability to the hepatocytes is essential for IGF-I gene expression. Protein malnutrition not only decreases IGF-I production rate, but also enhances its serum clearance and degradation. Finally, there is evidence for selective organ resistance to the growth-promoting effects of IGF-I in protein-restricted rats.

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☆ Supported by grants from the Fonds National de la Recherche Scientifique (3.4538.80, 3.4544.87, 3.4559.93, and 1.5.333.86F), Brussels, Belgium, National Institutes of Health (NIH) Grants No. HD26871 and HD08299, NIH Training Grant No. AM07129, and a NIH Fogarty International Fellowship (TW04384).

PII: 0026-0495(95)90221-X

Metabolism - Clinical and Experimental
Volume 44, Supplement 4 , Pages 50-57, October 1995

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