RGD Reference Report - Growth hormone-dependent regulation of pituitary GH secretagogue receptor (GHS-R) mRNA levels in the spontaneous dwarf Rat. - Rat Genome Database

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Growth hormone-dependent regulation of pituitary GH secretagogue receptor (GHS-R) mRNA levels in the spontaneous dwarf Rat.

Authors: Kamegai, J  Wakabayashi, I  Miyamoto, K  Unterman, T G  Kineman, R D  Frohman, L A 
Citation: Kamegai J, etal., Neuroendocrinology. 1998 Nov;68(5):312-8.
RGD ID: 12904721
Pubmed: PMID:9822798   (View Abstract at PubMed)

Growth hormone secretagogues (GHSs) are synthetic peptidyl and nonpeptidyl compounds that are believed to stimulate the release of GH by a direct effect on the pituitary somatotrope and by stimulation of growth hormone-releasing hormone (GHRH) release and the suppression of somatostatin (SRIH) tone. Recently, the receptor for these pharmacologic agents was cloned and its expression localized to the pituitary and hypothalamus. The elucidation of an unique GHS receptor (GHS-R) suggests there is a yet to be identified endogenous ligand which could exert an important role in regulation of GH secretion. It is clearly established that GH acts to regulate its own production by feeding back at the level of the hypothalamus to downregulate GHRH and upregulate SRIH synthesis and by induction of IGF-I, which acts at the pituitary to block somatotrope responsiveness to GHRH. If the endogenous GHS/GHS-R signaling system is important in regulating GH release, it might be reasoned that changes in circulating GH concentrations would also directly or indirectly (via generation of IGF-I) modify GHS-R production. To test this hypothesis we used RT-PCR to examined pituitary and hypothalamic GHS-R mRNA levels in the spontaneous dwarf rat (SDR), an animal model characterized by the absence of GH due to a point mutation in the GH gene. In the absence of GH feedback regulation, SDR pituitary GHS-R mRNA levels were 385 +/- 61% greater (p < 0.01) than those observed in normal controls while SDR hypothalamic GHS-R mRNA levels were not significantly different from those in normal rats. Three-day subcutaneous infusion of rat GH by osmotic pump reduced SDR pituitary GHS-R mRNA levels to 55 +/- 9% of vehicle-treated controls (p < 0.05) but did not significantly alter hypothalamic GHS-R mRNA levels. To test if the changes in GHS-R mRNA levels observed following GH treatment were due to elevation of circulating IGF-I concentrations, SDRs were infused with recombinant human IGF-I. Replacement of IGF-I did not significantly alter either pituitary or hypothalamic GHS-R mRNA levels, indicating that GH acts independent of circulating IGF-I to regulate pituitary GHS-R expression in the SDR model.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
isolated growth hormone deficiency  ISOGhsr (Rattus norvegicus)12904721; 12904721mRNA:increased expression:pituitary:RGD 
isolated growth hormone deficiency  IEP 12904721mRNA:increased expression:pituitary:RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to growth hormone  IEP 12904721 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ghsr  (growth hormone secretagogue receptor)

Genes (Mus musculus)
Ghsr  (growth hormone secretagogue receptor)

Genes (Homo sapiens)
GHSR  (growth hormone secretagogue receptor)


Additional Information