Ontogeny of growth hormone-releasing factor and its role in fetal and neonatal growth
The role of growth hormone (GH) in controlling postnatal growth is unquestioned (Underwood and Van Wyk 1981). The secretion of this hormone is in turn mediated by hypothalamic growth hormone-releasing factor (GRF; Guillemin et al. 1982; Rivier et al. 1982) and growth hormone-releasing inhibiting factor, also known as somatostatin (Brazeau et al. 1973). Under normal conditions the release of GH is episodic in nature. The variations in plasma GH concentrations cannot be explained by corresponding hypothalamic release of somatostatin, since infusion of antiserum raised against somatostatin does not abolish the pulses of GH secretion (Ferland et al. 1976; Terry and Martin 1981). It has now been demonstrated that the administration of antiserum raised against GRF abruptly abolishes GH pulses (Wehrenberg et al. 1982; Chihara et al. 1984). Furthemore, direct evidence suggests that GRF is released by the hypothalamus in an episodic fashion (Plotsky and Vale 1985). Thus, while somatostatin plays a role in modulating GH secretion, it appears that GRF is responsible for elevated GH concentrations and its pulsatile pattern of secretion. In light of this relationship and the clear role GH has in somatic growth, we became interested in the role of GRF in regulating somatic growth of the fetus and neonate. This review covers our current knowledge of the ontogeny of GRF and experiments we have conducted to evaluate its role in fetal and neonatal growth in the rat.
KeywordsCatheter Albumin Lactate Cage Morphine
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