| First Author | Frohman LA | Year | 1996 |
| Journal | Metabolism | Volume | 45 |
| Issue | 8 Suppl 1 | Pages | 1-3 |
| PubMed ID | 8769367 | Mgi Jnum | J:34913 |
| Mgi Id | MGI:82368 | Doi | 10.1016/s0026-0495(96)90067-0 |
| Citation | Frohman LA (1996) New insights into the regulation of somatotrope function using genetic and transgenic models. Metabolism 45(8 Suppl 1):1-3 |
| abstractText | Growth hormone (GH) secretion is under the control of the hypothalamic hormones GH-releasing hormone (GHRH) and somatostatin (SRIF), and is regulated by feedback effects of GH and insulin-like growth factor (IGF-1). GHRH End SRIF act on somatotropes by binding to G-protein-coupled receptors. GHRH activates the stimulatory G protein (GS), leading primarily to activation of adenylyl cyclase and protein kinase A. SRIF activates the inhibitory G protein (G(i)). Several animal models enable the study of various disorders of GH secretion in vivo. Genetic models of impaired GH Secretion include the little (lit) mouse, the dwarf (dw) rat, the fatty (fa) rat, and the high-growth (hg) mouse. Transgenic models of impaired and excessive GH secretion, respectively, include the tyrosine hydroxylase- human GH (TH-hGH) transgenic mouse and the metallothionein- human GHRH transgenic mouse. These models encompass a wide spectrum of disorders of GH secretion, involving defects of hypothalamic regulation, feedback control at the pituitary level, or the mechanism of GHRH action in the somatotrope. They may provide insights into our understanding of human GH secretory disorders. Copyright (C) 1996 by W.B. Saunders Company |
