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Article: Gene expression of hypothalamic somatostatin, growth hormone releasing factor, and their pituitary receptors in hypothyroidism

TitleGene expression of hypothalamic somatostatin, growth hormone releasing factor, and their pituitary receptors in hypothyroidism
Authors
Issue Date1996
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 1996, v. 137 n. 2, p. 418-424 How to Cite?
AbstractThyroid hormones are important to growth in mammals and have been shown to rapidly stimulate the rate of GH gene transcription. In this study, we investigated whether thyroid hormones modulate GH secretion through their effects on the gene expression of GRF, somatostatin (SS), GRF receptor, and receptor subtype 2 for SS (SSTR2). Male adult Sprague-Dawley rats were rendered hypothyroid with a single injection of propylthiouracil followed by methimazole in drinking water (0.02%) for 1 day to 12 weeks. Total RNA extracted from the anterior pituitary and hypothalamus was analyzed by Northern hybridization. GH messenger RNA (mRNA) level in the anterior pituitary was significantly reduced in the hypothyroid animals (P < 0.0001 vs. controls for all treatment duration ≥1 week). An increase in hypothalamic GRF mRNA level, by 2- and 4-fold, respectively, was seen after 3 and 12 weeks of antithyroid treatment (both P < 0.001 vs. controls). Hypothalamic GRF content, studied in 12-week hypothyroid rats only, was decreased compared with controls (P < 0.05). A reduction in pituitary GRF receptor mRNA level was observed after 1 week of antithyroid treatment (P < 0.01 after 1 week, P < 0.001 after 3 weeks). Total hypothalamic SS content and SS mRNA level in hypothalamic fragments consisting predominantly of the paraventricular and periventricular nuclei became significantly decreased (P < 0.05 and P < 0.005 respectively) after 12 weeks of antithyroid treatment. The reduction in SS gene expression in the periventricular nuclei was confirmed by in situ hybridization. No significant change in the mRNA level of pituitary SSTR2 was observed up to 12 weeks of antithyroid treatment. In conclusion, we have demonstrated a reduction in the gene expression of GRF receptor and SS in the hypothyroid rat. Our results suggest that the changes in hypothalamic GRF and SS gene expression in hypothyroid rats may be compensatory in nature and are likely to be secondary to the reduction in GH synthesis and secretion in these animals. The reduction in basal and GRF- stimulated GH secretion in hypothyroidism can be explained by the observed reduction in GH and GRF receptor gene expression.
Persistent Identifierhttp://hdl.handle.net/10722/49133
ISSN
2023 Impact Factor: 3.8
2023 SCImago Journal Rankings: 1.285
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTam, SPen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.date.accessioned2008-06-12T06:35:08Z-
dc.date.available2008-06-12T06:35:08Z-
dc.date.issued1996en_HK
dc.identifier.citationEndocrinology, 1996, v. 137 n. 2, p. 418-424en_HK
dc.identifier.issn0013-7227en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49133-
dc.description.abstractThyroid hormones are important to growth in mammals and have been shown to rapidly stimulate the rate of GH gene transcription. In this study, we investigated whether thyroid hormones modulate GH secretion through their effects on the gene expression of GRF, somatostatin (SS), GRF receptor, and receptor subtype 2 for SS (SSTR2). Male adult Sprague-Dawley rats were rendered hypothyroid with a single injection of propylthiouracil followed by methimazole in drinking water (0.02%) for 1 day to 12 weeks. Total RNA extracted from the anterior pituitary and hypothalamus was analyzed by Northern hybridization. GH messenger RNA (mRNA) level in the anterior pituitary was significantly reduced in the hypothyroid animals (P < 0.0001 vs. controls for all treatment duration ≥1 week). An increase in hypothalamic GRF mRNA level, by 2- and 4-fold, respectively, was seen after 3 and 12 weeks of antithyroid treatment (both P < 0.001 vs. controls). Hypothalamic GRF content, studied in 12-week hypothyroid rats only, was decreased compared with controls (P < 0.05). A reduction in pituitary GRF receptor mRNA level was observed after 1 week of antithyroid treatment (P < 0.01 after 1 week, P < 0.001 after 3 weeks). Total hypothalamic SS content and SS mRNA level in hypothalamic fragments consisting predominantly of the paraventricular and periventricular nuclei became significantly decreased (P < 0.05 and P < 0.005 respectively) after 12 weeks of antithyroid treatment. The reduction in SS gene expression in the periventricular nuclei was confirmed by in situ hybridization. No significant change in the mRNA level of pituitary SSTR2 was observed up to 12 weeks of antithyroid treatment. In conclusion, we have demonstrated a reduction in the gene expression of GRF receptor and SS in the hypothyroid rat. Our results suggest that the changes in hypothalamic GRF and SS gene expression in hypothyroid rats may be compensatory in nature and are likely to be secondary to the reduction in GH synthesis and secretion in these animals. The reduction in basal and GRF- stimulated GH secretion in hypothyroidism can be explained by the observed reduction in GH and GRF receptor gene expression.en_HK
dc.format.extent418 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_HK
dc.relation.ispartofEndocrinologyen_HK
dc.subject.meshGene Expressionen_HK
dc.subject.meshGrowth Hormone-Releasing Hormone - genetics - metabolismen_HK
dc.subject.meshHypothalamus - metabolismen_HK
dc.subject.meshHypothyroidism - genetics - metabolismen_HK
dc.subject.meshPituitary Gland, Anterior - metabolismen_HK
dc.titleGene expression of hypothalamic somatostatin, growth hormone releasing factor, and their pituitary receptors in hypothyroidismen_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_OA_fulltexten_HK
dc.identifier.doi10.1210/en.137.2.418en_HK
dc.identifier.pmid8593784-
dc.identifier.scopuseid_2-s2.0-0030038520en_HK
dc.identifier.hkuros9453-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030038520&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume137en_HK
dc.identifier.issue2en_HK
dc.identifier.spage418en_HK
dc.identifier.epage424en_HK
dc.identifier.isiWOS:A1996TR82600005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTam, SP=7202036931en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.issnl0013-7227-

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