The decrease in progesterone around parturition is generally agreed to be required for the onset of milk secretion. In humans, it is known that removal of the placenta, the source of progesterone, is necessary for the initiation of milk secretion. In swine, timing of the increase in milk lactose correlates closely with timing of the decrease in plasma progesterone at parturition. Exogenous progesterone prevents lactose and lipid synthesis in mammary glands of pregnant rats and sheep after removal of their ovaries, the source of progesterone in these species. Progesterone also suppresses ^-casein expression in the rat mammary gland during pregnancy and the decrease in progesterone levels is linked to increased ^-casein synthesis at parturition. Receptors for progesterone are not detected in lactating mammary tissues, which explains why progesterone does not inhibit established lactation. It is likely that the decline in progesterone is insufficient to activate secretion and that the actions of other hormones, including prolactin and glucocorticoids, are necessary to complete this process. In all in vitro mammary systems, insulin and corticoids, in addition to prolactin, are necessary to maintain synthesis of milk components. Further more, cortisol replacement is required for maintenance of milk production in adrenalectomized animals. An early notion that a surge of glucocorticoids is the initiator of lactation is likely incorrect since the increase in cortisol seen in unanesthetized women associated with the stress of labor is complete by the time milk volume begins to increase to any extent. Because secretory activation proceeds at parturition in severely diabetic rats, a role for insulin in lactogenesis as opposed to metabolic adjustments during lactation seems improbable. In summary, the most reasonable interpretation of the data from both animal and human studies is that the hormonal trigger for lactogenesis is a decrease in progesterone in the presence of maintained prolactin. Since postpartum prolactin levels are similar in both breast-feeding and non-breast-feeding women, the basic process appears to be initiated whether or not breast-feeding occurs. The caveat, of course, is that the mammary epithelium must be sufficiently prepared by the hormones of pregnancy to respond with milk synthesis.
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