Carolyn A. Bondy, MD; Louis E. Underwood, MD; David R. Clemmons, MD; Hans-Peter Guler, MD; Mark A. Bach, MD, PhD; Monica Skarulis, MD
Bondy CA, Underwood LE, Clemmons DR, Guler H, Bach MA, Skarulis M. Clinical Uses of Insulin-like Growth Factor I. Ann Intern Med. 1994;120:593-601. doi: 10.7326/0003-4819-120-7-199404010-00011
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Published: Ann Intern Med. 1994;120(7):593-601.
Insulin-like growth factor I (IGF-I) has acute insulin-like metabolic effects and long-term anabolic actions. The therapeutic potential of recombinant human IGF-I treatment is being investigated in various growth hormone-resistant and insulin-resistant disorders. Recent studies have shown that IGF-I may substitute for growth hormone in promoting linear growth in children with growth hormone insensitivity. The anabolic, protein-sparing action of IGF-I is being evaluated as a potential therapy for adults with catabolic diseases. Patients with insulin-dependent diabetes mellitus have reduced endogenous IGF-I production, and studies are in progress to determine whether treatment with IGF-I in addition to insulin may improve their metabolic/anabolic status. Insulin-like growth factor I treatment may reduce glucose and triglyceride levels in adults with non–insulin-dependent diabetes mellitus and in some patients with extreme insulin resistance. Further studies are needed to evaluate the efficacy and safety of IGF-I treatment in these and other conditions and to provide a better understanding of this hormone's normal physiologic role(s) and complex relations with growth hormone and insulin.
Growth hormone and insulin both stimulate hepatic IGF-I production, and IGF-I feeds back to suppress growth hormone and insulin release. Insulin-like growth factor-binding protein-3 (BP3) and the associated acid-labile subunit (ALS) levels are positively regulated by growth hormone, whereas IGF-binding protein-1 (BP1) levels are negatively regulated by insulin.
Under normal conditions, growth hormone secreted by the pituitary gland stimulates production of IGF-I by liver and other tissues. Insulin-like growth factor I, in turn, stimulates proliferation of cartilage, statural growth, and growth of other tissues. Insulin-like growth factor I exerts feedback suppression of growth hormone at the level of the hypothalamus and pituitary gland. In the Laron syndrome, defective growth hormone receptors cause unresponsiveness to growth hormone, low IGF-I levels, poor growth, and reduced feedback suppression of growth hormone secretion. The goal for treating such patients is to bypass the need for growth hormone by administering IGF-I. In patients with deletion of the growth hormone gene, growth hormone is sometimes ineffective as a long-term treatment for delayed growth because of the development of large amounts of antibodies that bind growth hormone in the circulation and inhibit its action. In these patients, administering IGF-I should bypass the need for growth hormone.
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