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dc.creatorMarsili, Alessandro
dc.creatorSánchez, Edith
dc.creatorSingru, Praful
dc.creatorHarney, John W.
dc.creatorZavacki, Ann Marie
dc.creatorLechan, Ronald M.
dc.creatorLarsen, P.R.
dc.date.accessioned2017-06-30T01:40:35Z
dc.date.available2017-06-30T01:40:35Z
dc.date.issued2011es_ES
dc.identifier1515es_ES
dc.identifier.issn0022-0795es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/6194
dc.identifier.urihttps://doi.org/10.1530/JOE-11-0248es_ES
dc.language.isoenges_ES
dc.relation211 (1) 73-78 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleThyroxine-induced expression of pyroglutamyl peptidase II and inhibition of TSH release precedes suppression of TRH mRNA and requires type 2 deiodinasees_ES
dc.typearticlees_ES
dc.contributor.affiliationThyroid Section, Division of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.es_ES
dc.contributor.emailplarsen@partners.orges_ES
dc.relation.jnabreviadoJ ENDOCRINOLes_ES
dc.relation.journalThe Journal of Endocrinologyes_ES
dc.identifier.placeInglaterraes_ES
dc.date.published2011es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1479-6805es_ES
dc.identifier.doi10.1530/JOE-11-0248es_ES
dc.description.monthOctes_ES
dc.description.abstractotrodiomaSuppression of TSH release from the hypothyroid thyrotrophs is one of the most rapid effects of 3,3',5'-triiodothyronine (T(3)) or thyroxine (T(4)). It is initiated within an hour, precedes the decrease in TSH_ mRNA inhibition and is blocked by inhibitors of mRNA or protein synthesis. TSH elevation in primary hypothyroidism requires both the loss of feedback inhibition by thyroid hormone in the thyrotrophs and the positive effects of TRH. Another event in this feedback regulation may be the thyroid hormone-mediated induction of the TRH-inactivating pyroglutamyl peptidase II (PPII) in the hypothalamic tanycytes. This study compared the chronology of the acute effects of T(3) or T(4) on TSH suppression, TRH mRNA in the hypothalamic paraventricular nucleus (PVN), and the induction of tanycyte PPII. In wild-type mice, T(3) or T(4) caused a 50% decrease in serum TSH in hypothyroid mice by 5_ h. There was no change in TRH mRNA in PVN over this interval, but there was a significant increase in PPII mRNA in the tanycytes. In mice with genetic inactivation of the type 2 iodothyronine deiodinase, T(3) decreased serum TSH and increased PPII mRNA levels, while T(4)-treatment was ineffective. We conclude that the rapid suppression of TSH in the hypothyroid mouse by T(3) occurs prior to a decrease in TRH mRNA though TRH inactivation may be occurring in the median eminence through the rapid induction of tanycyte PPII. The effect of T(4), but not T(3), requires the type 2 iodothyronine deiodinasees_ES
dc.subject.koAminopeptidaseses_ES
dc.subject.kometabolismes_ES
dc.subject.koAnimalses_ES
dc.subject.koAntithyroid Agentses_ES
dc.subject.koadverse effectses_ES
dc.subject.koDisease Models, Animales_ES
dc.subject.koHypothyroidismes_ES
dc.subject.kochemically inducedes_ES
dc.subject.koHypothyroidismes_ES
dc.subject.kometabolismes_ES
dc.subject.koInjections, Intraperitoneales_ES
dc.subject.koIodide Peroxidasees_ES
dc.subject.kogeneticses_ES
dc.subject.koIodide Peroxidasees_ES
dc.subject.kometabolismes_ES
dc.subject.koMicees_ES
dc.subject.koMice, Inbred C57BLes_ES
dc.subject.koMice, Knockoutes_ES
dc.subject.koParaventricular Hypothalamic Nucleuses_ES
dc.subject.kometabolismes_ES
dc.subject.koParaventricular Hypothalamic Nucleuses_ES
dc.subject.kopathologyes_ES
dc.subject.koPyrrolidonecarboxylic Acides_ES
dc.subject.koanalogs & derivativeses_ES
dc.subject.koPyrrolidonecarboxylic Acides_ES
dc.subject.kometabolismes_ES
dc.subject.koRNA, Messengeres_ES
dc.subject.koantagonists & inhibitorses_ES
dc.subject.koRNA, Messengeres_ES
dc.subject.kometabolismes_ES
dc.subject.koThyrotropines_ES
dc.subject.koantagonists & inhibitorses_ES
dc.subject.koThyrotropines_ES
dc.subject.kometabolismes_ES
dc.subject.koThyrotropin-Releasing Hormonees_ES
dc.subject.koantagonists & inhibitorses_ES
dc.subject.koThyrotropin-Releasing Hormonees_ES
dc.subject.kometabolismes_ES
dc.subject.koThyroxinees_ES
dc.subject.koadministration & dosagees_ES
dc.subject.koThyroxinees_ES
dc.subject.kopharmacologyes_ES
dc.subject.koTriiodothyroninees_ES
dc.subject.koadministration & dosagees_ES
dc.subject.koTriiodothyroninees_ES
dc.subject.kopharmacologyes_ES
dc.subject.koAntithyroid Agentses_ES
dc.subject.koRNA, Messengeres_ES
dc.subject.koThyrotropin-Releasing Hormonees_ES
dc.subject.koTriiodothyroninees_ES
dc.subject.koThyroxinees_ES
dc.subject.koThyrotropines_ES
dc.subject.koPyrrolidonecarboxylic Acides_ES
dc.subject.koiodothyronine deiodinase type IIes_ES
dc.subject.koIodide Peroxidasees_ES
dc.subject.koAminopeptidaseses_ES
dc.subject.kopyroglutamyl-peptidase IIes_ES


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