Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1996 Jul;1(3):307-15.
doi: 10.1007/BF02018083.

Feedback Control of Milk Secretion From Milk


Feedback Control of Milk Secretion From Milk

M Peaker et al. J Mammary Gland Biol Neoplasia. .


Extracellular storage allows biologically-active substances in milk to influence mammary function. Among these factors is one which regulates the rate of milk secretion acutely according to frequency or completeness of milk removal in each mammary gland. The active factor in goat's milk has been identified by screening milk constituents for their ability to inhibit milk constituent secretion in tissue and cell culture bioassays, and found to be a novel milk protein. The proteins identified by bioassy in vitro, also inhibited milk secretion in lactating goats in a reversible, concentration-dependent manner. This protein, termed FIL (feedback inhibitor of lactation), acts by reversible blockade of constitutive secretion in the mammary epithelial cell. As the inhibitor is synthesized in the same epithelial cells, feedback inhibition is, therefore, an autocrine mechanism. FIL's unusual mechanism of action also influences other aspects of mammary function. Acute disruption of mammary membrane trafficking is associated with downregulation of prolactin receptors and followed by a decrease in epithelial cell differentiation. Thus, in addition to acutely-regulating milk secretion, FIL may induce the adaptation in mammary cell differentiation which acts in vivo to sustain the secretory response to a sustained change in milk removal. In the long term, matching of milk output to demand is achieved by a change in mammary cell number. This developmental response is also local in nature. Whether it too is due to autocrine modulation by FIL of mechanisms influencing cell proliferation or survival, or elicited by another milk-borne factor, remains to be determined.

Similar articles

See all similar articles

Cited by 11 articles

See all "Cited by" articles


    1. Nature. 1993 Aug 26;364(6440):818-21 - PubMed
    1. Biochem J. 1995 Jan 1;305 ( Pt 1):51-8 - PubMed
    1. Science. 1991 Nov 22;254(5035):1197-9 - PubMed
    1. Int Rev Cytol. 1980;68:251-306 - PubMed
    1. Development. 1989 Feb;105(2):223-35 - PubMed

LinkOut - more resources