Subventions et des contributions :

Titre :
Remodeling of mammary tissue and lactation persistency
Numéro de l’entente :
RGPIN
Valeur d'entente :
125 000,00 $
Date d'entente :
10 mai 2017 -
Organisation :
Conseil de recherches en sciences naturelles et en génie du Canada
Location :
Québec, Autre, CA
Numéro de référence :
GC-2017-Q1-02648
Type d'entente :
subvention
Type de rapport :
Subventions et des contributions
Renseignements supplémentaires :

Subvention ou bourse octroyée s'appliquant à plus d'un exercice financier. (2017-2018 à 2022-2023)

Nom légal du bénéficiaire :
Lacasse, Pierre (Université de Sherbrooke)
Programme :
Programme de subventions à la découverte - individuelles
But du programme :

The long range objectives of this research program are to improve our knowledge of the biological process involved in the control of mammary gland involution and to develop economically viable and consumer acceptable technologies or practices that would improve lactation persistency and enable longer lactation in dairy cows. Extended lactation would reduce the proportion of cow’s lifetime spent in early lactation and, thus, the occurrence of disease, metabolic disorder and reproduction failure associated with this period.
Although little is known about the biological control of persistency, factors such as milking frequency, completeness of milk removal, parity, photoperiod, nutrient intake and gestation have been shown to affect it. Recent work carried out in my laboratory, have demonstrated that the hormone prolactin (PRL), contrary to what was believed, is galactopoietic in dairy ruminants. If basal level of PRL was not clearly associated with level of milk production, the milking-induced PRL release was correlated to level of milk production Anti-apoptotic effects of PRL have been reported in the mammary gland of rodents and, accordingly, we found more apoptosis in the glands of cows where PRL secretion was inhibited. Therefore, it is possible that PRL, especially the milking-induced PRL, is an important factor for lactation persistency by limiting the loss of cells and maintaining cell differentiation. However, we also found that the galactopoietic action of PRL is modulated at the level of the mammary gland by a mechanism that remains to be elucidated.

My hypotheses are:
-The milking-induced release of hormone is important to maintain the differentiation, the secretory activity and the survival of the mammary epithelial cells.
- Several factors affect milk production and lactation persistency by modulating the amount of hormones release at milking and/or mammary gland responsiveness to them.

My short range objectives are:
1- To determine the factors controling the magnitude of milking-induced release of PRL
2- To determine the mechanisms by which local factors affect lactation persistency.
3- To determine the mechanism(s) by which systemic factors affect lactation persistency