ACTH Blocker Master Data Weaner2020 pub data.xlsx
The hypothalamic–pituitary–adrenal (HPA) axis controls the release of glucocorticoids, which regulate immune and inflammatory function by modulating cytokines, white blood cells and oxidative stress via glucocorticoid receptor (GR) signaling. Although the response to HPA activation is well character...
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ftdatacite:10.6084/m9.figshare.16629148.v1 2023-05-15T16:05:23+02:00 ACTH Blocker Master Data Weaner2020 pub data.xlsx Ensminger, David 2021 https://dx.doi.org/10.6084/m9.figshare.16629148.v1 https://figshare.com/articles/dataset/ACTH_Blocker_Master_Data_Weaner2020_pub_data_xlsx/16629148/1 unknown figshare https://dx.doi.org/10.6084/m9.figshare.16629148 Creative Commons Attribution 4.0 International https://creativecommons.org/licenses/by/4.0/legalcode cc-by-4.0 CC-BY 60806 Animal Physiological Ecology FOS Biological sciences 60203 Ecological Physiology dataset Dataset 2021 ftdatacite https://doi.org/10.6084/m9.figshare.16629148.v1 https://doi.org/10.6084/m9.figshare.16629148 2021-11-05T12:55:41Z The hypothalamic–pituitary–adrenal (HPA) axis controls the release of glucocorticoids, which regulate immune and inflammatory function by modulating cytokines, white blood cells and oxidative stress via glucocorticoid receptor (GR) signaling. Although the response to HPA activation is well characterized in many species, little is known about the impacts of HPA activation during extreme physiological conditions. Hence, we challenged 18 simultaneously fasting and developing elephant seal pups with daily intramuscular injections of adrenocorticotropin (ACTH), a GR antagonist (RU486), or a combination of the two (ACTH+RU486) for 4 days. We collected blood at baseline, 2 h and 4 days after the beginning of treatment ACTH and ACTH+RU486 elevated serum aldosterone and cortisol at 2 h, with effects diminishing at 4 days. RU486 alone induced a compensatory increase in aldosterone, but not cortisol, at 4 days. ACTH decreased neutrophils at 2 h, while decreasing lymphocytes and increasing the neutrophil:lymphocyte ratio at 4 days. These effects were abolished by RU486. Despite alterations in white blood cells, there was no effect of ACTH or RU486 on transforming growth factor-β or interleukin-6 levels; however, both cytokines decreased with the 4 day fasting progression. Similarly, ACTH did not impact protein oxidation, lipid peroxidation or antioxidant enzymes, but plasma isoprostanes and catalase activity decreased while glutathione peroxidase increased with fasting progression. These data demonstrate differential acute (2 h) and chronic (4 days) modulatory effects of HPA activation on white blood cells and that the chronic effect is mediated, at least in part, by GR. These results also underscore elephant seals’ extraordinary resistance to oxidative stress derived from repeated HPA activation. Dataset Elephant Seal Elephant Seals DataCite Metadata Store (German National Library of Science and Technology) |
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DataCite Metadata Store (German National Library of Science and Technology) |
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unknown |
topic |
60806 Animal Physiological Ecology FOS Biological sciences 60203 Ecological Physiology |
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60806 Animal Physiological Ecology FOS Biological sciences 60203 Ecological Physiology Ensminger, David ACTH Blocker Master Data Weaner2020 pub data.xlsx |
topic_facet |
60806 Animal Physiological Ecology FOS Biological sciences 60203 Ecological Physiology |
description |
The hypothalamic–pituitary–adrenal (HPA) axis controls the release of glucocorticoids, which regulate immune and inflammatory function by modulating cytokines, white blood cells and oxidative stress via glucocorticoid receptor (GR) signaling. Although the response to HPA activation is well characterized in many species, little is known about the impacts of HPA activation during extreme physiological conditions. Hence, we challenged 18 simultaneously fasting and developing elephant seal pups with daily intramuscular injections of adrenocorticotropin (ACTH), a GR antagonist (RU486), or a combination of the two (ACTH+RU486) for 4 days. We collected blood at baseline, 2 h and 4 days after the beginning of treatment ACTH and ACTH+RU486 elevated serum aldosterone and cortisol at 2 h, with effects diminishing at 4 days. RU486 alone induced a compensatory increase in aldosterone, but not cortisol, at 4 days. ACTH decreased neutrophils at 2 h, while decreasing lymphocytes and increasing the neutrophil:lymphocyte ratio at 4 days. These effects were abolished by RU486. Despite alterations in white blood cells, there was no effect of ACTH or RU486 on transforming growth factor-β or interleukin-6 levels; however, both cytokines decreased with the 4 day fasting progression. Similarly, ACTH did not impact protein oxidation, lipid peroxidation or antioxidant enzymes, but plasma isoprostanes and catalase activity decreased while glutathione peroxidase increased with fasting progression. These data demonstrate differential acute (2 h) and chronic (4 days) modulatory effects of HPA activation on white blood cells and that the chronic effect is mediated, at least in part, by GR. These results also underscore elephant seals’ extraordinary resistance to oxidative stress derived from repeated HPA activation. |
format |
Dataset |
author |
Ensminger, David |
author_facet |
Ensminger, David |
author_sort |
Ensminger, David |
title |
ACTH Blocker Master Data Weaner2020 pub data.xlsx |
title_short |
ACTH Blocker Master Data Weaner2020 pub data.xlsx |
title_full |
ACTH Blocker Master Data Weaner2020 pub data.xlsx |
title_fullStr |
ACTH Blocker Master Data Weaner2020 pub data.xlsx |
title_full_unstemmed |
ACTH Blocker Master Data Weaner2020 pub data.xlsx |
title_sort |
acth blocker master data weaner2020 pub data.xlsx |
publisher |
figshare |
publishDate |
2021 |
url |
https://dx.doi.org/10.6084/m9.figshare.16629148.v1 https://figshare.com/articles/dataset/ACTH_Blocker_Master_Data_Weaner2020_pub_data_xlsx/16629148/1 |
genre |
Elephant Seal Elephant Seals |
genre_facet |
Elephant Seal Elephant Seals |
op_relation |
https://dx.doi.org/10.6084/m9.figshare.16629148 |
op_rights |
Creative Commons Attribution 4.0 International https://creativecommons.org/licenses/by/4.0/legalcode cc-by-4.0 |
op_rightsnorm |
CC-BY |
op_doi |
https://doi.org/10.6084/m9.figshare.16629148.v1 https://doi.org/10.6084/m9.figshare.16629148 |
_version_ |
1766401279415812096 |