Comment

The textbook view of the hormonal control of the release of growth hormone (GH) from the anterior pituitary gland is that it is exerted in two principally different ways. There are two releasing factors emanating from nerve nuclei in the hypothalamus: growth hormone releasing hormone and somatostatin, the latter hormone inhibiting the release of GH. Furthermore, circulating insulin-like growth factor (IGF) I, the release of which is controlled by GH, functions together with GH itself as negative feedback factors with regard to secretion of GH. Hence with increasing plasma levels of IGF-I and/or GH, the release of GH is inhibited.1

In 1984 a synthetic hexapeptide, containing two D-amino acid residues, was demonstrated to cause the release of GH.2Subsequently, it was shown that this peptide and other non-peptidergic GH secretagogues (GHSs) did not act via any of the known cell membrane receptors controlling GH secretion. The effect of GHS on GH release was “physiological”—that is, the increased GH secretion exhibited in the normal pulsatile pattern. Using molecular biology techniques it was possible to …