Ghrelin and GHRP-6-induced ACTH and cortisol release in thyrotoxicosis
dc.contributor.author | Nascif, Sergio Oliva [UNIFESP] | |
dc.contributor.author | Molica, Patricia [UNIFESP] | |
dc.contributor.author | Correa-Silva, Silvia Regina [UNIFESP] | |
dc.contributor.author | Silva, Marcos Roberto [UNIFESP] | |
dc.contributor.author | Lengyel, Ana-Maria Judith [UNIFESP] | |
dc.contributor.institution | Universidade Federal de São Paulo (UNIFESP) | |
dc.date.accessioned | 2016-01-24T13:58:57Z | |
dc.date.available | 2016-01-24T13:58:57Z | |
dc.date.issued | 2009-12-01 | |
dc.description.abstract | Thyrotoxicosis might alter the hypothalamic-pituitary-adrenal (HPA) axis. We evaluated the effects of ghrelin and GHRP-6 on the HPA axis in 20 hyperthyroid patients and in 9 controls. Mean basal cortisol (mu g/dl) and ACTH (pg/ml) levels were higher in hyperthyroidism (cortisol: 10.7 +/- A 0.7; ACTH: 21.5 +/- A 2.9) compared to controls (cortisol: 8.1 +/- A 0.7; ACTH: 13.5 +/- A 1.8). in thyrotoxicosis a dagger AUC cortisol values (mu g/dl.90 min) after ghrelin (484 +/- A 80) and GHRP-6 (115 +/- A 63) were similar to controls (ghrelin: 524 +/- A 107; GHRP-6: 192 +/- A 73). A significant increase in a dagger AUC ACTH (pg/ml.90 min) after ghrelin was observed in thyrotoxicosis (4,189 +/- A 1,202) compared to controls (1,499 +/- A 338). a dagger AUC ACTH values after GHRP-6 were also higher, although not significantly (patients: 927 +/- A 330; controls: 539 +/- A 237). in summary, our results suggest that ghrelin-mediated pathways of ACTH release might be activated by thyroid hormone excess, but adrenocortical reserve is maintained. | en |
dc.description.affiliation | Universidade Federal de São Paulo, Div Endocrinol, EPM, BR-04039002 São Paulo, Brazil | |
dc.description.affiliationUnifesp | Universidade Federal de São Paulo, Div Endocrinol, EPM, BR-04039002 São Paulo, Brazil | |
dc.description.source | Web of Science | |
dc.description.sponsorship | Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) | |
dc.description.sponsorship | Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) | |
dc.format.extent | 315-321 | |
dc.identifier | http://dx.doi.org/10.1007/s11102-009-0181-3 | |
dc.identifier.citation | Pituitary. New York: Springer, v. 12, n. 4, p. 315-321, 2009. | |
dc.identifier.doi | 10.1007/s11102-009-0181-3 | |
dc.identifier.issn | 1386-341X | |
dc.identifier.uri | http://repositorio.unifesp.br/handle/11600/31982 | |
dc.identifier.wos | WOS:000270977600006 | |
dc.language.iso | eng | |
dc.publisher | Springer | |
dc.relation.ispartof | Pituitary | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.rights.license | http://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0 | |
dc.subject | Ghrelin | en |
dc.subject | ACTH | en |
dc.subject | Cortisol | en |
dc.subject | Thyrotoxicosis | en |
dc.title | Ghrelin and GHRP-6-induced ACTH and cortisol release in thyrotoxicosis | en |
dc.type | info:eu-repo/semantics/article |