Review: Inhibition of prolactin as a management tool in dairy husbandry


Lacasse, P., Zhao, X., Vanacker, N., Boutinaud, M. (2019). Review: Inhibition of prolactin as a management tool in dairy husbandry. Animal, [online] 13(S1), S35-S41.

Plain language summary

Although the role of the hormone prolactin in dairy ruminants has been controversial for many years, this review presents recent evidence that prolactin is galactopoietic (induces the formation and secretion of milk) in ruminant lactation. We also discuss how prolactin modulation could be used as a management tool to improve energy balance during the postpartum period and during acute nutritional stress as well as to facilitate drying-off.


Accumulating evidence supports that the hormone prolactin (PRL) is galactopoietic in dairy ruminants. Accordingly, the inhibition of PRL secretion by the dopamine agonists quinagolide and cabergoline causes a sharp decline in milk production and could be useful in several critical periods. First, PRL inhibition may reduce the incidence during the periparturient period of metabolic disorders caused by the abrupt increase in energy demand for milk production. Metabolic disturbances can be lessened by reducing milk output by milking once a day or incompletely in the first few days of lactation. The injection of cows with quinagolide for the first 4 days of lactation reduced milk production during the first week of lactation without any residual effects. Blood glucose and calcium concentrations were higher and β-hydroxybutyric acid concentration was lower in the quinagolide-treated cows. Second, PRL inhibition may help sick or injured lactating cows, considering that they can fall into severe negative energy balance when they are unable to consume enough feed to support their milk production. This leads to a weakened immune system and increased susceptibility to diseases. When cows were subjected to feed restriction and were treated with quinagolide, the decrease in milk production was accelerated without any residual effects. The quinagolide-treated cows had higher glucose and lower β-hydroxybutyric acid and non-esterified fatty acid concentrations than the control cows did. Third, PRL inhibition may facilitate drying-off in high-yielding cows, because they are often dried off while still producing significant quantities of milk, which delays mammary involution and increases risk of mastitis. Therefore, strategies that reduce milk production before drying-off and accelerate mammary gland involution could be an important management tool. In this context, inhibition of PRL was utilised to accelerate mammary gland dry-off. Quinagolide decreased milk production within the first day of treatment, and both quinagolide and cabergoline induced more rapid changes in several markers of mammary gland involution after drying-off. In addition, quinagolide improved the animals' resistance to intramammary infection. These results suggest that the inhibition of PRL could be a strategy for facilitating drying-off, reducing metabolic stress during the postpartum period, and alleviating acute nutritional stress during illness without compromising the overall productivity of dairy ruminants.

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