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Hormonal Changes Associated With Lactogenesis

Hormone
Changes
Piglets suckling a sow.

Hormonal Changes Associated With Lactogenesis

A number of hormonal changes are occurring in the mother's blood around the time of parturition (see the figure below). Some of these hormonal changes are specifically involved in lactogenesis. From the figure, progesterone decreases starting a few days prepartum. Estrogen starts to peak prepartum, which in turn stimulates the periparturitent prolactin secretion. The periparurient prolactin peak is very important to the entire process of lactogensis, especially in initiating copius milk secretion (stage 2 of lactogenesis). Glucocorticoids also peak at parturition. And, there is a growth hormone peak associated with parturition. The content of a-lactalbumin in the mammary tissue is an indicator of lactogenesis.

Graph of hormone changes around parturition.
Adapted from Tucker (1994)

** Progesterone is the key negative regulator of lactogenesis.

  • Progesterone has a negative (inhibitory) effect on lactogenesis. It may hold lactogenesis in check until just prior to parturition.
  • Progesterone suppresses normal peripartum onset of synthesis of lactose, a-lactalbumin and casein as well as PRL-induced synthesis of these constituents.
  • If progesterone concentrations in blood are reduced during the peripartum period, then the synthesis of mammary enzymes and milk proteins is increased.
  • Blood concentrations of progesterone normally decrease about 2 days prepartum.
  • Progesterone also may compete with glucocorticoid for glucocorticoid receptors in the mammary cells.
  • High progesterone concentrations during pregnancy may occupy glucocorticoid receptors until near parturition.

In vivo , progesterone probably works by a) increasing the mammary threshold to response to PRL (there are progesterone receptors in the mammary gland during pregnancy, so it can have a direct effect on the mammary cells); b) altering secretion of PRL from the pituitary; and c) having a direct effect on the mammary cells by occupying glucocorticoid receptors.
 
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