FEMALES
- a mixture of estrogens of which 17β-estradiol is the most abundant (and most potent).
- progesterone.
- are primarily responsible for the conversion of girls into sexually-mature women.
- development of breasts
- further development of the uterus and vagina
- broadening of the pelvis
- growth of pubic and axillary hair
- increase in adipose (fat) tissue
- participate in the monthly preparation of the body for a possible pregnancy
- participate in pregnancy if it occurs
Estrogens also have non-reproductive effects.
- They antagonize the effects of the parathyroid hormone, minimizing the loss of calcium from bones and thus helping to keep bones strong.
- They promote blood clotting.
Steroids like estrogens and progesterone are small, hydrophobic molecules that are transported in the blood bound to a serum globulin.
- In "target" cells, i.e., cells that change their gene expression in response to the hormone, they bind to receptor proteins located in the cytoplasm and/or nucleus.
- The hormone-receptor complex enters the nucleus (if it formed in the cytoplasm) and
- binds to specific sequences of DNA, called the estrogen (or progesterone) response elements
- Response elements are located in the promoters of genes.
- The hormone-receptor complex acts as a transcription factor (often recruiting other transcription factors to help) which
- turns on (sometimes off) transcription of those genes.
- Gene expression in the cell produces the response.
The synthesis and secretion of estrogens is stimulated by follicle-stimulating hormone (FSH), which is, in turn, controlled by the hypothalamic gonadotropin releasing hormone (GnRH).
Hypothalamus | → | GnRH | → | Pituitary | → | FSH | → | Follicle | → | Estrogens |
It works like this: Secretion of GnRH depends on certain neurons in the hypothalamus which express a gene (KiSS-1) encoding a protein of 145 amino acids. From this are cut several short peptides collectively called kisspeptin. These are secreted and bind to G-protein-coupled receptors on the surface of the GnRH neurons stimulating them to release GnRH. However, high levels of estrogen (or progesterone or testosterone) inhibit the secretion of kisspeptin and suppress further production of those hormones.
Progesterone production is stimulated by luteinizing hormone (LH), which is also stimulated by GnRH.
Hypothalamus | → | GnRH | → | Pituitary | → | LH | → | Corpus luteum | → | Progesterone |
Elevated levels of progesterone control themselves by the same negative feedback loop used by estrogen (and testosterone).
The Menstrual Cycle
- The rising level of estrogen causes the endometrium to become thicker and more richly supplied with blood vessels and glands.
- A rising level of LH causes the developing egg within the follicle to complete the first meiotic division (meiosis I), forming a secondary oocyte.
- After about two weeks, there is a sudden surge in the production of LH.
- This surge in LH triggers ovulation: the release of the secondary oocyte into the fallopian tube.
- Under the continued influence of LH, the now-empty follicle develops into a corpus luteum (hence the name luteinizing hormone for LH).
- Stimulated by LH, the corpus luteum secretes progesterone which
- continues the preparation of the endometrium for a possible pregnancy
- inhibits the contraction of the uterus
- inhibits the development of a new follicle
- If fertilization does not occur (which is usually the case),
- the rising level of progesterone inhibits the release of GnRH which, in turn,
- inhibits further production of progesterone.
- As the progesterone level drops,
- the corpus luteum begins to degenerate;
- the endometrium begins to break down, its cells committing programmed cell death (apoptosis);
- the inhibition of uterine contraction is lifted, and
- the bleeding and cramps of menstruation begin.
MALES
The principal androgen (male sex hormone) is testosterone. This steroid is manufactured by the interstitial (Leydig) cells of the testes. Secretion of testosterone increases sharply at puberty and is responsible for the development of the so-called secondary sexual characteristics (e.g., beard) of men. Testosterone is also essential for the production of sperm.
Production of testosterone is controlled by the release of luteinizing hormone (LH) from the anterior lobe of the pituitary gland, which is in turn controlled by the release of GnRH from the hypothalamus. LH is also called interstitial cell stimulating hormone (ICSH).
Hypothalamus | → | GnRH | → | Pituitary | → | LH | → | Testes | → | Testosterone |
The level of testosterone is under negative-feedback control: a rising level of testosterone suppresses the release of GnRH from the hypothalamus. This is exactly parallel to the control of estrogen secretion in females. [Look back]
Males need estrogen, too!
In 1994, a man was described who was homozygous for a mutation in the gene encoding the estrogen receptor. A single nonsense mutation had converted a codon (CGA) for arginine early in the protein into a STOP codon (TGA). Thus no complete estrogen receptor could be synthesized.This man was extra tall, had osteoporosis and "knock-knees", but was otherwise well. His genetic defect confirms the important role that estrogen has in both sexes for normal bone development.
It is not known whether this man (or any of the few other men who have been found with the same disorder) is fertile or not. However, an article in the 4 December 1997 issue of Nature reports that male mice whose estrogen receptor gene has been "knocked out" are sterile.
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