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Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release
Growth hormone (GH) regulates whole body metabolism, and physical exercise is the most potent stimulus to induce its secretion in humans. The mechanisms underlying GH secretion after exercise remain to be defined. The aim of this study was to elucidate the role of estrogen and pituitary type 1 deiod...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4395113/ https://www.ncbi.nlm.nih.gov/pubmed/25874614 http://dx.doi.org/10.1371/journal.pone.0122556 |
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author | Ignacio, Daniele Leão da S. Silvestre, Diego H. Cavalcanti-de-Albuquerque, João Paulo Albuquerque Louzada, Ruy Andrade Carvalho, Denise P. Werneck-de-Castro, João Pedro |
author_facet | Ignacio, Daniele Leão da S. Silvestre, Diego H. Cavalcanti-de-Albuquerque, João Paulo Albuquerque Louzada, Ruy Andrade Carvalho, Denise P. Werneck-de-Castro, João Pedro |
author_sort | Ignacio, Daniele Leão |
collection | PubMed |
description | Growth hormone (GH) regulates whole body metabolism, and physical exercise is the most potent stimulus to induce its secretion in humans. The mechanisms underlying GH secretion after exercise remain to be defined. The aim of this study was to elucidate the role of estrogen and pituitary type 1 deiodinase (D1) activation on exercise-induced GH secretion. Ten days after bilateral ovariectomy, animals were submitted to 20 min of treadmill exercise at 75% of maximum aerobic capacity and tissues were harvested immediately or 30 min after exercise. Non-exercised animals were used as controls. A significant increase in D1 activity occurred immediately after exercise (~60%) in sham-operated animals and GH was higher (~6-fold) 30 min after exercise. Estrogen deficient rats exhibited basal levels of GH and D1 activity comparable to those found in control rats. However, after exercise both D1 activity and serum GH levels were blunted compared to sedentary rats. To understand the potential cause-effect of D1 activation in exercise-induced GH release, we pharmacologically blocked D1 activity by propylthiouracil (PTU) injection into intact rats and submitted them to the acute exercise session. D1 inhibition blocked exercise-induced GH secretion, although basal levels were unaltered. In conclusion, estrogen deficiency impairs the induction of thyroid hormone activating enzyme D1 in the pituitary, and GH release by acute exercise. Also, acute D1 activation is essential for exercise-induced GH response. |
format | Online Article Text |
id | pubmed-4395113 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-43951132015-04-21 Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release Ignacio, Daniele Leão da S. Silvestre, Diego H. Cavalcanti-de-Albuquerque, João Paulo Albuquerque Louzada, Ruy Andrade Carvalho, Denise P. Werneck-de-Castro, João Pedro PLoS One Research Article Growth hormone (GH) regulates whole body metabolism, and physical exercise is the most potent stimulus to induce its secretion in humans. The mechanisms underlying GH secretion after exercise remain to be defined. The aim of this study was to elucidate the role of estrogen and pituitary type 1 deiodinase (D1) activation on exercise-induced GH secretion. Ten days after bilateral ovariectomy, animals were submitted to 20 min of treadmill exercise at 75% of maximum aerobic capacity and tissues were harvested immediately or 30 min after exercise. Non-exercised animals were used as controls. A significant increase in D1 activity occurred immediately after exercise (~60%) in sham-operated animals and GH was higher (~6-fold) 30 min after exercise. Estrogen deficient rats exhibited basal levels of GH and D1 activity comparable to those found in control rats. However, after exercise both D1 activity and serum GH levels were blunted compared to sedentary rats. To understand the potential cause-effect of D1 activation in exercise-induced GH release, we pharmacologically blocked D1 activity by propylthiouracil (PTU) injection into intact rats and submitted them to the acute exercise session. D1 inhibition blocked exercise-induced GH secretion, although basal levels were unaltered. In conclusion, estrogen deficiency impairs the induction of thyroid hormone activating enzyme D1 in the pituitary, and GH release by acute exercise. Also, acute D1 activation is essential for exercise-induced GH response. Public Library of Science 2015-04-13 /pmc/articles/PMC4395113/ /pubmed/25874614 http://dx.doi.org/10.1371/journal.pone.0122556 Text en © 2015 Ignacio et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Ignacio, Daniele Leão da S. Silvestre, Diego H. Cavalcanti-de-Albuquerque, João Paulo Albuquerque Louzada, Ruy Andrade Carvalho, Denise P. Werneck-de-Castro, João Pedro Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release |
title | Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release |
title_full | Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release |
title_fullStr | Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release |
title_full_unstemmed | Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release |
title_short | Thyroid Hormone and Estrogen Regulate Exercise-Induced Growth Hormone Release |
title_sort | thyroid hormone and estrogen regulate exercise-induced growth hormone release |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4395113/ https://www.ncbi.nlm.nih.gov/pubmed/25874614 http://dx.doi.org/10.1371/journal.pone.0122556 |
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