I found an explanation in 

Pang, Hartman J Mammary Gland Biol Neoplasia 2007 12:211-221 'Initiation of Human Lactation: Secretory Differentiation and Secretory Activation:



'Glucocorticoid receptors are present in the cytosol of

mammary epithelial cells and when bound to glucocorticoids,

the receptors translocate to the nucleus and act

synergistically with prolactin-activated transcription factors

to enable the synthesis of milk proteins, such as, casein and

α-lactalbumin. While progesterone binds to the glucocorticoid

receptor, it does not then translocate to the nucleus

and activate the milk protein genes [49]. Although the

affinity of the binding of progesterone to the glucocorticoid

receptor is lower than that of the glucocorticoids, the free

concentrations of progesterone are much higher than the

glucocorticoids during pregnancy [9, 61–63]. Thus progesterone

may displace the glucocorticoids binding from the

glucocorticoid receptor during pregnancy. This competition

for the glucocorticoid receptor may ensure that secretion

from the mammary gland is minimal as it develops its

secretory capacity during pregnancy. On the other hand,

others have concluded that the progesterone receptor itself is

responsible for progesterone’s inhibition of milk synthesis

during pregnancy.



In other words, the progesterone is binding to glucocorticoid receptors, not PRL receptors. When progesterone is bound to these receptors, PRL-activated transcription factors cannot enable the synthesis of milk proteins, which is crucial to make milk.



Anne





Anne Eglash MD, IBCLC, FABM

Clinical Professor, Department of Family and Community Medicine

University of Wisconsin School of Medicine and Public Health

Medical Director, UW Lactation Services

Medical Director, Mothers Milk Bank of the Western Great Lakes

Founder and President of The Milk Mob, dedicated to building Breastfeeding Knowledgeable Medical Systems and Communities http://www.themilkmob.org











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