The hormones of estrogens, progestogens, prolactin and androgens influence breast tissue through Estrogen Receptor Alpha (ERα), Progesterone Receptor B (PRB), and Prolactin Receptor (PrlR). Estrogen Receptor Beta (ERβ) in the reproductive tract is important for estrogen balance. 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 secretory phase
Of ERα, PRB, and PrlR, mild potencies of their non-respective hormone enhances each hormone receptor'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.
Estrogens are formed from androgens through a process called aromatase, and aromatase enzymes are located within tissue where ERα and ERβ are also present. This includes ovarian, egg, bone, brain and adipose tissue. Function of theca cells, which produce androgens, and granulosa cells, which produce estrogens, within the follicle or corpus luteum are together important for reproductive health.
The menstrual cycle will be divided into 5 phases to simply timing: menstruation, proliferative, ovulation, secretory and premenstrual. During menstruation, follicle stimulating hormone (FSH) increases menstruation intensity, and prolactin decreases menstruation intensity. Estrogen is not the dominant hormone for menstruation. During proliferative phase, estrogen levels rise, which develops the egg, and prepares the reproductive tract for it. Estrogen suppresses Luteinizing Hormone (LH) at first, but a buildup of estrogen eventually causes the body to release LH. LH allows ovulation to occur, releasing the egg from the ovary, leaving behind the corpus luteum. The sequential rise of LH, then FSH initially matures the corpus luteum within the ovary during ovulation. FSH then pushes the egg towards the uterus. Progesterone is produced by the corpus luteum, which is a temporary organ whose function is to signal the pituitary gland to momentarily prevent menstruation, for purposes of maintaining fertilization or pregnancy. Lower amounts of estrogens than progestogens are produced during the luteal phase and pregnancy. The pituitary gland releases prolactin, which signals the corpus luteum (and if during pregnancy, the placenta) to release more progesterone, creating a feedback loop. Progesterone increases prolactin, and prolactin lowers FSH and LH. If the egg is not fertilized, the corpus luteum withers within the ovaries. Once progesterone levels drop during premenstrual phase, the pituitary gland signals the release of FSH, allowing menstruation to begin. Outside of the secretory phase, premenstrual phase or pregnancy, progesterone amounts in the body are existant (due to the adrenal glands), but negligible.
This is the outdated version of chapter 1 from breast-endocrinology.pdf. The next chapter is Hormone Imbalances. super-bazongas.pdf continues on herb use.
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