Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status

Abstract Thyroid disorders cause abnormal puberty, indicating interactions between the hypothalamus-pituitary-thyroid (HPT) and hypothalamus-pituitary-gonadal (HPG) axes, which are important in pubertal development. The hypothalamic gonadotropin-inhibitory hormone (GnIH) was shown to be decreased in...

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Autores principales:	Mika Kiyohara, You Lee Son, Kazuyoshi Tsutsui
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b46362d05214469699a96b8b5866641b
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spelling	oai:doaj.org-article:b46362d05214469699a96b8b5866641b2021-12-02T16:05:59ZInvolvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status10.1038/s41598-017-01183-82045-2322https://doaj.org/article/b46362d05214469699a96b8b5866641b2017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01183-8https://doaj.org/toc/2045-2322Abstract Thyroid disorders cause abnormal puberty, indicating interactions between the hypothalamus-pituitary-thyroid (HPT) and hypothalamus-pituitary-gonadal (HPG) axes, which are important in pubertal development. The hypothalamic gonadotropin-inhibitory hormone (GnIH) was shown to be decreased in the early prepubertal stage, suggesting the role of GnIH on pubertal onset. Here, we investigated whether thyroid dysfunction affects pubertal onset in female mice via GnIH regulation. Hypothyroidism showed delayed pubertal onset with increased GnIH expression and reduced pituitary-gonadal activity. Remarkably, knockout of GnIH prevented the effect of hypothyroidism to delay the pubertal onset, resulting in indistinguishable pubertal timing in GnIH-knockout female mice between control and hypothyroidism-induced group, indicating that increased GnIH expression induced by hypothyroidism may lead to delayed puberty. In contrast, hyperthyroidism led to a decrease in GnIH expression, however pubertal onset was normal, implying further reduction of the inhibitory GnIH had little effect on the phenotypical change. Critically, thyroid hormone suppressed GnIH expression in hypothalamic explants and GnIH neurons expressed thyroid hormone receptors to convey the thyroid status. Moreover, the thyroid status highly regulated the chromatin modifications of GnIH promoter, H3acetylation and H3K9tri-methylation. These findings indicate a novel function of GnIH to mediate HPT-HPG interactions that contribute to proper pubertal development.Mika KiyoharaYou Lee SonKazuyoshi TsutsuiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Mika Kiyohara You Lee Son Kazuyoshi Tsutsui Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status
description	Abstract Thyroid disorders cause abnormal puberty, indicating interactions between the hypothalamus-pituitary-thyroid (HPT) and hypothalamus-pituitary-gonadal (HPG) axes, which are important in pubertal development. The hypothalamic gonadotropin-inhibitory hormone (GnIH) was shown to be decreased in the early prepubertal stage, suggesting the role of GnIH on pubertal onset. Here, we investigated whether thyroid dysfunction affects pubertal onset in female mice via GnIH regulation. Hypothyroidism showed delayed pubertal onset with increased GnIH expression and reduced pituitary-gonadal activity. Remarkably, knockout of GnIH prevented the effect of hypothyroidism to delay the pubertal onset, resulting in indistinguishable pubertal timing in GnIH-knockout female mice between control and hypothyroidism-induced group, indicating that increased GnIH expression induced by hypothyroidism may lead to delayed puberty. In contrast, hyperthyroidism led to a decrease in GnIH expression, however pubertal onset was normal, implying further reduction of the inhibitory GnIH had little effect on the phenotypical change. Critically, thyroid hormone suppressed GnIH expression in hypothalamic explants and GnIH neurons expressed thyroid hormone receptors to convey the thyroid status. Moreover, the thyroid status highly regulated the chromatin modifications of GnIH promoter, H3acetylation and H3K9tri-methylation. These findings indicate a novel function of GnIH to mediate HPT-HPG interactions that contribute to proper pubertal development.
format	article
author	Mika Kiyohara You Lee Son Kazuyoshi Tsutsui
author_facet	Mika Kiyohara You Lee Son Kazuyoshi Tsutsui
author_sort	Mika Kiyohara
title	Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status
title_short	Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status
title_full	Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status
title_fullStr	Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status
title_full_unstemmed	Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status
title_sort	involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/b46362d05214469699a96b8b5866641b
work_keys_str_mv	AT mikakiyohara involvementofgonadotropininhibitoryhormoneinpubertaldisordersinducedbythyroidstatus AT youleeson involvementofgonadotropininhibitoryhormoneinpubertaldisordersinducedbythyroidstatus AT kazuyoshitsutsui involvementofgonadotropininhibitoryhormoneinpubertaldisordersinducedbythyroidstatus
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Involvement of gonadotropin-inhibitory hormone in pubertal disorders induced by thyroid status

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