Abstract
The rate of milk secretion in the mammary gland is regulated by a complex interaction of peptide and steroid hormones. These hormones, and growth hormone in particular, have been the target of immunological manipulation in dairy animals aimed at controlling milk production. Recently, it has become clear that milk secretion is also regulated by a local mechanism operating within the mammary gland, which modulates the rate of secretion according to frequency and completeness of milk removal. We have shown that this occurs through feedback inhibition by a milk constituent, and have identified a novel milk protein in goat’s milk able to inhibit milk secretion in vivo and in vitro in a concentration-dependent, reversible manner. The protein has been named FIL (Feedback Inhibitor of Lactation), and since it is synthesised in the mammary epithelial cell along with other milk constituents, feedback inhibition is considered an autocrine mechanism. The autocrine mechanism was targetted in lactating goats, which were immunized against FIL three times in declining lactation. After the third immunization, when antibodies against FIL were consistently detected in milk, the decline in milk secretion was significantly reduced compared with sham-immunized controls. Immunization also reduced significantly the fall in milk yield due to once daily milking. These studies show that feedback inhibition is an important determinant of milk secretion rate in lactating animals, and indicate that this local mechanism can be manipulated immunologically to control the productivity of the dairy animal.
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© 1999 Kluwer Academic Publishers
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Wilde, C.J., Addey, C., Campbell, F., Peaker, M. (1999). Immunological Manipulation of Lactation. In: Kitagawa, Y., Matsuda, T., Iijima, S. (eds) Animal Cell Technology: Basic & Applied Aspects., vol 1. Springer, Dordrecht. https://doi.org/10.1007/0-306-46865-4_10
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DOI: https://doi.org/10.1007/0-306-46865-4_10
Publisher Name: Springer, Dordrecht
Print ISBN: 978-0-7923-5451-2
Online ISBN: 978-0-306-46865-0
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