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Article: Gene expression of hypothalamic somatostatin and growth hormone-releasing hormone in dexamethasone-treated rats

TitleGene expression of hypothalamic somatostatin and growth hormone-releasing hormone in dexamethasone-treated rats
Authors
KeywordsAdrenal steroids
Growth hormone
Growth hormone-releasing hormone
Molecular neuroendocrinology
Somatostatin
Issue Date1997
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEN
Citation
Neuroendocrinology, 1997, v. 66 n. 1, p. 2-8 How to Cite?
AbstractSupraphysiological doses of glucocorticoids inhibit growth hormone (GH) secretion in man and experimental animals. We investigated whether glucocorticoids inhibit GH secretion through changes in the gene expression of GH, hypothalamic somatostatin (SS) and GH-releasing hormone (GHRH), and whether such changes vary with the dose and duration of glucocorticoid excess. Male rats, 6 weeks of age, were treated with injections of either saline or different doses of dexamethasone (40, 200, 500 or 1000 μg/kg/day) intraperitoneally for 3 or 8 days. Total RNA extracted from the anterior pituitary and hypothalamus was analyzed by Northern blot hybridization. SS mRNA level was also assessed in smaller hypothalamic fragments containing predominantly the periventricular and paraventricular nuclei, and by in situ hybridization. A biphasic effect on SS mRNA levels was observed such that a significant increase (p < 0.001) was demonstrated in the periventricular nucleus after 3 days of dexamethasone 1000 μg/kg/day, but a reduction in hypothalamic SS mRNA was seen after 8 days for all doses employed (p < 0.05 or p < 0.01). On the other hand, hypothalamic GHRH mRNA levels showed a reduction which appeared to increase with the dose and duration of treatment and became statistically significant after 8 days at doses ≤ 200 μg/kg/day (p < 0.05). Pituitary GH mRNA levels were increased after 3 days at doses ≤ 500 μg/kg/day (p < 0.05) but showed no significant change at all doses after 8 days. We conclude that glucocorticold excess is associated with changes in the gene expression of GH, hypothalamic SS and GHRH, which vary with the dose and duration of glucocorticoid treatment. Glucocorticoids inhibit GH secretion in vivo through a reduction in hypothalamic GHRH gene expression and, in animals with shorter duration of glucocorticoid excess, also through an increase in SS gene expression in the periventricular nucleus.
Persistent Identifierhttp://hdl.handle.net/10722/148085
ISSN
2015 Impact Factor: 2.583
2015 SCImago Journal Rankings: 1.479
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.date.accessioned2012-05-29T06:10:45Z-
dc.date.available2012-05-29T06:10:45Z-
dc.date.issued1997en_HK
dc.identifier.citationNeuroendocrinology, 1997, v. 66 n. 1, p. 2-8en_HK
dc.identifier.issn0028-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148085-
dc.description.abstractSupraphysiological doses of glucocorticoids inhibit growth hormone (GH) secretion in man and experimental animals. We investigated whether glucocorticoids inhibit GH secretion through changes in the gene expression of GH, hypothalamic somatostatin (SS) and GH-releasing hormone (GHRH), and whether such changes vary with the dose and duration of glucocorticoid excess. Male rats, 6 weeks of age, were treated with injections of either saline or different doses of dexamethasone (40, 200, 500 or 1000 μg/kg/day) intraperitoneally for 3 or 8 days. Total RNA extracted from the anterior pituitary and hypothalamus was analyzed by Northern blot hybridization. SS mRNA level was also assessed in smaller hypothalamic fragments containing predominantly the periventricular and paraventricular nuclei, and by in situ hybridization. A biphasic effect on SS mRNA levels was observed such that a significant increase (p < 0.001) was demonstrated in the periventricular nucleus after 3 days of dexamethasone 1000 μg/kg/day, but a reduction in hypothalamic SS mRNA was seen after 8 days for all doses employed (p < 0.05 or p < 0.01). On the other hand, hypothalamic GHRH mRNA levels showed a reduction which appeared to increase with the dose and duration of treatment and became statistically significant after 8 days at doses ≤ 200 μg/kg/day (p < 0.05). Pituitary GH mRNA levels were increased after 3 days at doses ≤ 500 μg/kg/day (p < 0.05) but showed no significant change at all doses after 8 days. We conclude that glucocorticold excess is associated with changes in the gene expression of GH, hypothalamic SS and GHRH, which vary with the dose and duration of glucocorticoid treatment. Glucocorticoids inhibit GH secretion in vivo through a reduction in hypothalamic GHRH gene expression and, in animals with shorter duration of glucocorticoid excess, also through an increase in SS gene expression in the periventricular nucleus.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NENen_HK
dc.relation.ispartofNeuroendocrinologyen_HK
dc.rightsNeuroendocrinology. Copyright © S Karger AG.-
dc.subjectAdrenal steroidsen_HK
dc.subjectGrowth hormoneen_HK
dc.subjectGrowth hormone-releasing hormoneen_HK
dc.subjectMolecular neuroendocrinologyen_HK
dc.subjectSomatostatinen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Northernen_US
dc.subject.meshDexamethasone - Administration & Dosage - Pharmacologyen_US
dc.subject.meshGene Expression - Drug Effectsen_US
dc.subject.meshGlucocorticoids - Pharmacologyen_US
dc.subject.meshGrowth Hormone - Blood - Geneticsen_US
dc.subject.meshGrowth Hormone-Releasing Hormone - Geneticsen_US
dc.subject.meshHypothalamus - Chemistry - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshPituitary Gland, Anterior - Chemistryen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSomatostatin - Geneticsen_US
dc.titleGene expression of hypothalamic somatostatin and growth hormone-releasing hormone in dexamethasone-treated ratsen_HK
dc.typeArticleen_HK
dc.identifier.emailLam, KSL:ksllam@hku.hken_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9258913-
dc.identifier.scopuseid_2-s2.0-0030915729en_HK
dc.identifier.hkuros33565-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030915729&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume66en_HK
dc.identifier.issue1en_HK
dc.identifier.spage2en_HK
dc.identifier.epage8en_HK
dc.identifier.isiWOS:A1997XL30000001-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK

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