Clinical Implications of Growth Hormone Release Inhibiting Hormone (GH-RIH)
GH-RIH (or somatostatin) “was isolated as a cyclic tetradeca-peptide” by Guillemin and his colleagues in 1973, and shown to inhibit growth hormone (GH) release in sheep in vivo and from isolated human acromegalic pituitary cells, in vitro, Brazeau et al. (1973). Shortly afterwards, it was shown in in vivo studies in normal human subjects to suppress secretion of GH in response to all known stimuli, including insulin-induced hypoglycaemia, 1-dopa, arginine, exercise and sleep (Hall 1973; Hansen et al., 1973; Mortimer et al., 1974; Siler et al., 1974). Surprisingly, even in normal subjects, the pituitary effects were not limited to actions on GH since TSH secretion after TRH was impaired although prolactin release after TRH was not reduced (Hall et al., 1973). This material did not affect pituitary LH, FSH or ACTH secretion. However, in addition to the actions on the pituitary, GH-RIH was shown to alter other hormonal secretions in normal subjects. Thus, pancreatic glucagon and insulin secretion were suppressed, as were gastrin, acid and pepsin secretion from the stomach (Mortimer et al., 1974; Alberti et al., 1974; Bloom et al., 1974; Gomez-Pan et al., 1975). There are preliminary studies suggesting that renin secretion can also be suppressed, but that parathyroid hormone secretion is not.
KeywordsGrowth Hormone Growth Hormone Level Acromegalic Patient Glucagon Level Supar Level
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