The hormones of estrogens, progestogens, and prolactin influence breast tissue through Estrogen Receptor Alpha (ERα), Progesterone Receptor B (PRB), and Prolactin Receptor (PrlR). As each receptor is positively stimulated by its respective hormone, it also becomes desensitized. There are more receptor types in the breast that cannot be ignored due to health reasons, but those mentioned above regulate breast tissue.
Positive estrogenic stimulation, or agonism, of ERα causes lengthening of milk ducts. Branching of milk ducts, which increases the amount of end buds, is caused by progestogenic agonism on PRB. The initial formation of milk lobules converted from the end of milk ducts and their continued growth is caused by prolactin’s effects on PrlR. Progesterone also has a role in differentiation, or conversion of end points into milk lobules, by influencing prolactin, during the luteal phase.
Of ERα, PRB, and PrlR, their non-respective hormone enhances each hormone's response to its respective hormone, known as receptor upregulation. Without this synergistic action, the response to a receptor's own specific hormone dulls with quantity or potency, known as receptor downregulation. Too much of a potent hormone may possibly damage its own and other interacting receptors. An imbalance of too much of one type of hormone is a cancer risk. The breast contains more types of cell receptors, but the mentioned above are the focus here.
This is an excerpt. Read breast-endocrinology.pdf or super-bazongas.pdf for more.
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- Premenstrual Breast Changes. ADAM Encyclopedia. July 2015. https://www.nlm.nih.gov/medlineplus/ency/article/003153.htm.
- Mammary Gland. Encyclopædia Britannica. 2012. .
- Steroid Hormone. Encyclopædia Britannica. 2012. .
- Super Bazongas. https://breast.is/ebook/super-bazongas.pdf.