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

@article{Kamegai1998GrowthHR,
  title={Growth hormone-dependent regulation of pituitary GH secretagogue receptor (GHS-R) mRNA levels in the spontaneous dwarf Rat.},
  author={Jun Kamegai and Ichiji Wakabayashi and Ken-Ichi Miyamoto and Terry G. Unterman and Rhonda D. Kineman and Lawrence A. Frohman},
  journal={Neuroendocrinology},
  year={1998},
  volume={68 5},
  pages={312-8}
}
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… CONTINUE READING

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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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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 .
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