Cellular Physiology of Growth Hormone Releasing Hormone
This chapter reviews the mechanisms involved in the normal transduction of the signal generated by binding of growth hormone (GH) releasing hormone (GHRH) to its receptor on the somatotropes in relation to GH secretion, GH synthesis, and cellular proliferation. This chapter also discusses the consequences of altered signal transduction, citing models of both genetic and transgenic origin with both decreased and increased activity of the system.
KeywordsGrowth Hormone Adenylyl Cyclase Cholera Toxin Pituitary Cell Altered Signal Transduction
Unable to display preview. Download preview PDF.
- 13.Jansson J, Downs TR, Beamer WG, Frohman LA. The dwarf “little” (lit/lit) mouse is resistant to growth hormone (GH)-releasing peptide (GH-RP-6) as well as to GH-releasing hormone (GRH). Program 68th Annual Meeting of the Endocrine Society, 1986;#397(abstr).Google Scholar
- 17.Zeitler PA, Downs TR, Frohman LA. Development of pituitary cell types in the spontaneous dwarf (dw) rat: evidence for an isolated defect in somatotroph differentiation. Endocrine 1994;2:729–33.Google Scholar
- 18.Pinhas-Hamiel O, Zeitler P. Impaired response to GHRP-6 in somatotrophs from dwarf (dw) rats. Program 76th Annual Meeting of the Endocrinc Society 1994;#663(abstr).Google Scholar
- 21.Frohman LA, Thominet JL, Szabo M. Ectopic growth hormone releasing factor syndromes. In: Raiti S, Tolman R, eds. Human growth hormone. New York: Plenum, 1986:347–60.Google Scholar
- 25.Spada A, Arosio M, Bochicchio D, Bazzoni N, Vallar L, Bassetti M, et al. Clinical, biochemical, and morphological correlates in patients bearing growth hormone-secreting pituitary tumors with or without constitutively active adenylyl cyclase. J Clin Endocrinol Metab 1990;71:1421–6.PubMedCrossRefGoogle Scholar