Confused about progesterone levels during the menstrual cycle...

[CBG23]

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So, I am reviewing the menstrual cycle and going for an understanding of the changes rather than flat out memorizing it and am a bit confused about Porgesterone levels during the cycle.

Basically, why don't progesterone levels rise during the follicular phase, but rise in the luteal phase?

In the follicular phase, you have theca interna cells being stimulated by LH --> increased activity of cholesterol desmolase --> would expect increased progesterone as well as increased DHEA, which is ultimately converted to Testosterone and then estrogen (under the influence of FSH) in the adjacent granulosa cells. In reality, only Estrogen levels rise during this phase.

In the luteal phase, you have the same deal except the cells have different names now: LH stimulates cholesterol desmolase in theca lutein cells --> would expect increased progesterone as well as increased DHEA, which is ultimately converted to Testosterone and then estrogen (under the influence of FSH) in the adjacent granulosa lutein cells. In reality,both Progesterone AND estrogen rise during this phase.

I looked in a couple of physiology books and this isn't really explained. Anybody understand the "why" behind this?

 

[OveractiveBrain]

Confused about progesterone levels during the menstrual cycle...

So is everyone else

 

[normtheniner]

So, I am reviewing the menstrual cycle and going for an understanding of the changes rather than flat out memorizing it and am a bit confused about Porgesterone levels during the cycle.

Basically, why don't progesterone levels rise during the follicular phase, but rise in the luteal phase?

In the follicular phase, you have theca interna cells being stimulated by LH --> increased activity of cholesterol desmolase --> would expect increased progesterone as well as increased DHEA, which is ultimately converted to Testosterone and then estrogen (under the influence of FSH) in the adjacent granulosa cells. In reality, only Estrogen levels rise during this phase.

In the luteal phase, you have the same deal except the cells have different names now: LH stimulates cholesterol desmolase in theca lutein cells --> would expect increased progesterone as well as increased DHEA, which is ultimately converted to Testosterone and then estrogen (under the influence of FSH) in the adjacent granulosa lutein cells. In reality,both Progesterone AND estrogen rise during this phase.

I looked in a couple of physiology books and this isn't really explained. Anybody understand the "why" behind this?

I wrote this summary for my friends a while back, maybe it'll be helpful. Took me a while to get the whole menstrual cycle...




Day 1-4: Menstruation -- Characterized by sloughing off of the stratum functionalis in the endometrium of the uterus, while the stratum basale remains unaffected. Blood exits the uterus and is released through vagina.

Day 5-~14: A surge in FSH from the pituitary gland induces the follicular or proliferative phase. This is characterized in the fallopian tube as well, this is when Ciliated cells are dominant. During the follicular phase, the endometrium is re-synthesized and uterine glands that will eventually produce glycogen begin to form and take on a STRAIGHT appearance. The estrogen being released by the follicles in the ovary is what drives this phase. In late follicular phase the glands take on a more tortuous appearance.

(Additional info I found helpful to understanding -- an alpha receptor for estrogen in the pituitary gland negatively inhibits the production of LH. Eventually, the threshold for estrogen is so high that another receptor (the beta receptor) triggers the release of LH leading to....)

Day 14: Ovulation

Day 14-27: LH stimulates the development of the Corpus Luteum from the ruptured ovarian follicle. The Corpus Luteum will secrete estrogen from the theca lutein and progesterone from the theca granulosa. This surge in hormone furthers the development of the endometrium and the arteries and glands that are going into it. Additionally, the Luteal phase (secretory phase) is characterized by Peg cell dominance in the fallopian tube.

The estrogen and progesterone eventually result in a negative feedback on the pituitary gland resulting in the gradual involution of the corpus luteum and the beginning of another menstrual cycle.



This was a beast to memorize... sorry if I got the details wrong or this isn't helpful...

 

[robu058]

So, I am reviewing the menstrual cycle and going for an understanding of the changes rather than flat out memorizing it and am a bit confused about Porgesterone levels during the cycle.

Basically, why don't progesterone levels rise during the follicular phase, but rise in the luteal phase?

In the follicular phase, you have theca interna cells being stimulated by LH --> increased activity of cholesterol desmolase --> would expect increased progesterone as well as increased DHEA, which is ultimately converted to Testosterone and then estrogen (under the influence of FSH) in the adjacent granulosa cells. In reality, only Estrogen levels rise during this phase.

In the luteal phase, you have the same deal except the cells have different names now: LH stimulates cholesterol desmolase in theca lutein cells --> would expect increased progesterone as well as increased DHEA, which is ultimately converted to Testosterone and then estrogen (under the influence of FSH) in the adjacent granulosa lutein cells. In reality,both Progesterone AND estrogen rise during this phase.

I looked in a couple of physiology books and this isn't really explained. Anybody understand the "why" behind this?

This is what happens during menstrual cycle.

Day 1-5: Have already been explained on the board but understand that it is the loss of progesterone that somehow induces uterine contraction. During contraction, the cells in the stratum functionalis in the endometrium shear and die, releasing their contents that include PGE2. Recall that prostaglandin E2 induces pain, and it is that pain female associates with cramp.

Day 5-~14: Initially, the hypothalamus releases GnRH. It then acts on Ant. Pituitary to induce the secretion of FSH/LH in a pulsatile fashion. LH activates an enzyme in the theca interna cells called "cholesterol desmolase," which converts cholesterol into pregnelonome.

Pregnelonome can give rise to many byproducts, including progesterone and androgen. Understand that Theca cells do not have the enzyme, aromatase, to convert androgen into estrogen. As a result, it secretes androgen and this molecule finds its way in the granulosa cells. There, FSH activates the aromatase enzyme previously mentioned, which allow the conversion of androgen into estrogen.

As a growth factor, the function of estrogen is to act on striatum basali, a type of stem cell, in the endotremium to induce proliferation of these cells. Thus, this stage is called proliferative stage.

In the meantime, the low level of estrogen has a negative effect on the ant. pituitary: it inhibits it. However, once the level of estrogen reaches a critical concentration, it no longer has the inhibition effect. Rather, it has a stimulated effect, promoting the released of a boat load of LH (LH surge). Recalls that LH acts on theca cells whereas FSH acts on granulosa cells. If the LH level is way greater than FSH, the pathway will favor more progesterone than estrogen.

In general, Progesterone ANTAGONIZEs the action of estrogen, and in this case it stops the proliferation of the endometrium glands in the uterus. Additionally, it prepare the uterus for possible implantation. This is called preparation phase or secretory phase, a phase where the egg will be released or secreted. Once the egg is released, we have ovulation.

Day 14: Ovulation

Day 15-27: Follow discussion on the board!


Hope the above explanation helps!!

 

[alysp13751]

Idk if this will help but Im going to try and explain it in an easy way:


-First half of the cycle 1-13 days:
It is called estrogenic phase in reference to the concentration of this hormone in blood, follicular phase in reference to the ovaries and proliferative stage in reference to the uterus.
The arcuate nucleus and the pre optic nucleus of the hypothalamus will release Gonadotropin releasing factor, and through a vascular connection it will reach the anterior pituitary gland. When certain cells in the anterior pituitary get stimulated they release gonadotropic hormones, this is FSH and LH.
The primordial follicles found in the ovaries do not need to be stimulated, they automatically start growing and become primary follicles without FSH help. Around 15 primordial follicles start growing automatically and some will become primary follicles. FSH helps primary follicles convert into secondary follicles.
So the reason why FSH concentration is so high in the first half of the cycle is because after the menstrual bleeding that is the first day of the cycle, gonadotropins are relased by the anterior pituitary to start a new cycle, primary follicles need to be stimulated to grow into secondary follicles hence the FSH.
Theca interna cells produce androgens that are sent to granulosa cells which covert them into ESTROGEN. This estrogen makes the endometrium to proliferate, but also due to the high concentration of estrogen in blood the anterior pituitary gland stops releasing FSH, because the fact that there is a high concentration of estrogen means enough primary follicles have matured, no need to release more FSH.

-Day 14 is ovulation day and for some reason we dont know the LH concentration increases dramatically. Estrogen is supposed to inhibit the production of FSH and LH but LH increases dramatically in what is called LH search.

- Second half of the cycle, from day 15 to 28.
Ok, in short, progesterone is being produced by corpus luteum in the ovary, whos gonna produce it for 13 days regardless of pregnancy or not. If there is pregnancy, HCG produced by the syncytiotrophoblasts will reach the corpus luteum and corpus luteum will become corpus luteum of pregnancy, it will produce much more progesterone and the endometrium will be in secretory stage, meaning the functional layers in which the conceptus is going to be embedded (compact and spongy layer) are present. Estrogen concentration will also be up, but nowhere as high as progesterone. The progesterone is what keeps the endometrium in secretory phase, which means menstrual bleeding will not occur (only occurs when there is no pregnancy, corpus luteum becomes corpus albincans and degenerates, there is no progesterone production, the progesterone that was keeping the vessels open in the functional endometrium will undergo splasticity later on will become necreotic and it will be discharged with some bleeding from the venules that are open.

I am just studying embryology though, no physiology, so this was prob useless, but good review anyways 🙂