Document Detail


Feedback control of milk secretion from milk.
MedLine Citation:
PMID:  10887504     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
M Peaker; C J Wilde
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Journal of mammary gland biology and neoplasia     Volume:  1     ISSN:  1083-3021     ISO Abbreviation:  J Mammary Gland Biol Neoplasia     Publication Date:  1996 Jul 
Date Detail:
Created Date:  2000-07-24     Completed Date:  2000-07-24     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  9601804     Medline TA:  J Mammary Gland Biol Neoplasia     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  307-15     Citation Subset:  IM    
Affiliation:
Hannah Research Institute, United Kingdom.
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MeSH Terms
Descriptor/Qualifier:
Animals
Breast / physiology*
Breast Feeding*
Feedback
Female
Humans
Lactation / physiology*
Mammary Glands, Animal / physiology*
Milk
Milk, Human

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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