Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.14.16.2 (tyrosine hydroxylase)
 14,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurons synthesizing growth hormone releasing factor were detected by immunocytochemistry with specific antiserum against synthetic rat hypothalamic growth hormone releasing factor. Growth hormone releasing factor immunoreactive neurons which also showed tyrosine hydroxylase immunoreactivity were located in the ventrolateral part of the arcuate nucleus. The functional significance of this finding for anterior pituitary hormone secretion is discussed.
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PMID:Coexistence of growth hormone releasing factor-like and tyrosine hydroxylase-like immunoreactivities in neurons of the rat arcuate nucleus. 286 50

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 and 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 (Gi). 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.
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PMID:New insights into the regulation of somatotrope function using genetic and transgenic models. 876 67

Growth hormone secretagogues (GHSs) stimulate GH secretion and food intake. GHS receptor (GHS-R) mRNA has been identified mainly in the arcuate nucleus (Arc) and ventromedial nucleus of the hypothalamus and in the pituitary. Ghrelin, an endogenous ligand for GHS-R, has recently been purified from rat stomach. Although ghrelin is also expressed in the hypothalamus, the physiological significance of the ghrelin/GHS-R system is still unknown. We have created transgenic (Tg) rats expressing an antisense GHS-R mRNA under the control of the promoter for tyrosine hydroxylase (TH), thus selectively attenuating GHS-R protein expression in the Arc. Tg rats had lower body weight and less adipose tissue than did control rats. Daily food intake was reduced, and the stimulatory effect of GHS treatment on feeding was abolished in Tg rats. GH secretion and plasma insulin-like growth factor-I levels were reduced in female Tg rats. These results suggest that GHS-R in the Arc is involved in the regulation of GH secretion, food intake, and adiposity.
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PMID:Hypothalamic growth hormone secretagogue receptor regulates growth hormone secretion, feeding, and adiposity. 1204 56