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GH, IGFs, IGF-binding protein-3 and acid-labile subunit: what is the pecking order?

Is the title of this Commentary a question which is still relevant? The dependence of insulin-like growth factor-I (IGF-I) on growth hormone (GH), which formed the basis of the classical somatomedin hypothesis (1), is now almost old hat. After insulin-like growth factorbinding protein-3 (IGFBP-3) was identified in serum as the carrier protein for most circulating IGFs, its variations were shown also to be regulated by GH secretion (2, 3). Serum ALS (acid-labile subunit), which binds IGFBP-3 associated with IGF-I or -II to form 140 kDa complexes (4), is age- and GH-dependent in the same way as are IGF-I and IGFBP-3. However, over recent years, the use of recombinant IGF-I in both experimental investigation and treatment of dwarfism resulting from genetic disorders of the GH receptor (Laron syndrome) has raised controversy as to the respective physiological roles of GH and IGF-I. It was recently proclaimed that ‘long-term IGF-I therapy in patients with Laron syndrome consistently failed to demonstrate any increase in IGFBP-3 concentrations, indicating that IGFBP-3 production is under the direct control of GH’ (5). With equal conviction, another group has concluded in this issue of the European Journal