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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.

Silanikove N, Shapiro F, Shinder D - BMC Physiol. (2009)

Bottom Line: 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 beta-casein (beta-CN (1-28)).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 beta-CN (1-28) is part of the regulatory system.

View Article: PubMed Central - HTML - PubMed

Affiliation: Biology of Lactation Laboratory, Inst, of Animal Sciences, Agricultural Research Organization, Bet Dagan 50250, Israel. nsilanik@agri.huji.ac.il

ABSTRACT

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 beta-casein (beta-CN (1-28)). These metabolites constitute the regulatory negative feedback system. Previously, it has been shown that beta-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 beta-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 beta-CN (1-28) is part of the regulatory system.

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Effects on K+ uptake into the vesicles, of all combinations of incubating infranatant (milk serum devoid of vesicles and casein micelles) with milk serum-derived vesicles sampled from the control cows at the morning milking and experimental cows at the noon milking. All combinations differed significantly at P < 0.01.
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Figure 3: Effects on K+ uptake into the vesicles, of all combinations of incubating infranatant (milk serum devoid of vesicles and casein micelles) with milk serum-derived vesicles sampled from the control cows at the morning milking and experimental cows at the noon milking. All combinations differed significantly at P < 0.01.

Mentions: Figure 3 depicts the results of K+ uptake determinations; it presents comparisons of all possible combinations of Inf and SMV sampled from the control cows at the morning milking with those sampled at midday from the experimental cows. The combination of Inf and SMV sampled from the morning milking of the control cows (Cinf-CSMV) served as the reference value. Inhibition of K+ uptake into the vesicles diminished in the order: Einf-ESMV > Einf-CSMV > Cinf - ESMV, with values of 52, 68 and 77% of Cinf-CSMV, respectively. The data in Figure 3 are consistent with those in Figure 2, which shows that acute heat stress increased the concentration of K+ channel blocker in the milk serum in proportion to the heat stress level. However, the data also indicate that vesicles (SMV) coming from heat-stressed cows were more responsive to the activity of the K+ channel blocker.


Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system.

Silanikove N, Shapiro F, Shinder D - BMC Physiol. (2009)

Effects on K+ uptake into the vesicles, of all combinations of incubating infranatant (milk serum devoid of vesicles and casein micelles) with milk serum-derived vesicles sampled from the control cows at the morning milking and experimental cows at the noon milking. All combinations differed significantly at P < 0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2714494&req=5

Figure 3: Effects on K+ uptake into the vesicles, of all combinations of incubating infranatant (milk serum devoid of vesicles and casein micelles) with milk serum-derived vesicles sampled from the control cows at the morning milking and experimental cows at the noon milking. All combinations differed significantly at P < 0.01.
Mentions: Figure 3 depicts the results of K+ uptake determinations; it presents comparisons of all possible combinations of Inf and SMV sampled from the control cows at the morning milking with those sampled at midday from the experimental cows. The combination of Inf and SMV sampled from the morning milking of the control cows (Cinf-CSMV) served as the reference value. Inhibition of K+ uptake into the vesicles diminished in the order: Einf-ESMV > Einf-CSMV > Cinf - ESMV, with values of 52, 68 and 77% of Cinf-CSMV, respectively. The data in Figure 3 are consistent with those in Figure 2, which shows that acute heat stress increased the concentration of K+ channel blocker in the milk serum in proportion to the heat stress level. However, the data also indicate that vesicles (SMV) coming from heat-stressed cows were more responsive to the activity of the K+ channel blocker.

Bottom Line: 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 beta-casein (beta-CN (1-28)).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 beta-CN (1-28) is part of the regulatory system.

View Article: PubMed Central - HTML - PubMed

Affiliation: Biology of Lactation Laboratory, Inst, of Animal Sciences, Agricultural Research Organization, Bet Dagan 50250, Israel. nsilanik@agri.huji.ac.il

ABSTRACT

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 beta-casein (beta-CN (1-28)). These metabolites constitute the regulatory negative feedback system. Previously, it has been shown that beta-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 beta-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 beta-CN (1-28) is part of the regulatory system.

Show MeSH
Related in: MedlinePlus