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Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system
BACKGROUND: The objective of this study was to determine if acute heat stress (HS) decreases milk secretion by activating the milk-borne negative feedback system, as an emergency physiological response to prevent a life-threatening situation. To induce HS, summer acclimatized dairy cows were exposed...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2009
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714494/ https://www.ncbi.nlm.nih.gov/pubmed/19563620 http://dx.doi.org/10.1186/1472-6793-9-13 |
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author | Silanikove, Nissim Shapiro, Fira Shinder, Dima |
author_facet | Silanikove, Nissim Shapiro, Fira Shinder, Dima |
author_sort | Silanikove, Nissim |
collection | PubMed |
description | BACKGROUND: The objective of this study was to determine if acute heat stress (HS) decreases milk secretion by activating the milk-borne negative feedback system, as an emergency physiological response to prevent a life-threatening situation. To induce HS, summer acclimatized dairy cows were exposed to full sun under mid-summer Mediterranean conditions, with and without conventional cooling procedures. RESULTS: Exposure to HS induced a rapid and acute (within 24 h) reduction in milk yield in proportion to the heat load. This decrease was moderated by cooler night-time ambient temperature. The reduction in milk yield was associated with corresponding responses in plasminogen activator/plasminogen-plasmin activities, and with increased activity (concentration) of the (1–28) N-terminal fragment peptide that is released by plasmin from β-casein (β-CN (1–28)). These metabolites constitute the regulatory negative feedback system. Previously, it has been shown that β-CN (1–28) down-regulated milk secretion by blocking potassium channels on the apical aspects of the mammary epithelial cells. CONCLUSION: Here we demonstrate that the potassium channels in mammary tissue became more susceptible to β-CN (1–28) activity under HS. Thus, the present study highlighted two previously unreported features of this regulatory system: (i) that it modulates rapidly in response to stressor impact variations; and (ii) that the regulations of the mammary epithelial potassium channel sensitivity to the inhibitory effect of β-CN (1–28) is part of the regulatory system. |
format | Text |
id | pubmed-2714494 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-27144942009-07-24 Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system Silanikove, Nissim Shapiro, Fira Shinder, Dima BMC Physiol Research Article BACKGROUND: The objective of this study was to determine if acute heat stress (HS) decreases milk secretion by activating the milk-borne negative feedback system, as an emergency physiological response to prevent a life-threatening situation. To induce HS, summer acclimatized dairy cows were exposed to full sun under mid-summer Mediterranean conditions, with and without conventional cooling procedures. RESULTS: Exposure to HS induced a rapid and acute (within 24 h) reduction in milk yield in proportion to the heat load. This decrease was moderated by cooler night-time ambient temperature. The reduction in milk yield was associated with corresponding responses in plasminogen activator/plasminogen-plasmin activities, and with increased activity (concentration) of the (1–28) N-terminal fragment peptide that is released by plasmin from β-casein (β-CN (1–28)). These metabolites constitute the regulatory negative feedback system. Previously, it has been shown that β-CN (1–28) down-regulated milk secretion by blocking potassium channels on the apical aspects of the mammary epithelial cells. CONCLUSION: Here we demonstrate that the potassium channels in mammary tissue became more susceptible to β-CN (1–28) activity under HS. Thus, the present study highlighted two previously unreported features of this regulatory system: (i) that it modulates rapidly in response to stressor impact variations; and (ii) that the regulations of the mammary epithelial potassium channel sensitivity to the inhibitory effect of β-CN (1–28) is part of the regulatory system. BioMed Central 2009-06-29 /pmc/articles/PMC2714494/ /pubmed/19563620 http://dx.doi.org/10.1186/1472-6793-9-13 Text en Copyright © 2009 Silanikove et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Silanikove, Nissim Shapiro, Fira Shinder, Dima Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system |
title | Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system |
title_full | Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system |
title_fullStr | Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system |
title_full_unstemmed | Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system |
title_short | Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system |
title_sort | acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714494/ https://www.ncbi.nlm.nih.gov/pubmed/19563620 http://dx.doi.org/10.1186/1472-6793-9-13 |
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