<P> In females: ovulation, maintaining of corpus luteum and secretion of progesterone . </P> <P> In males: testosterone secretion . </P> <P> LH supports theca cells in the ovaries that provide androgens and hormonal precursors for estradiol production . At the time of menstruation, FSH initiates follicular growth, specifically affecting granulosa cells . With the rise in estrogens, LH receptors are also expressed on the maturing follicle, which causes it to produce more estradiol . Eventually, when the follicle has fully matured, a spike in 17α - hydroxyprogesterone production by the follicle inhibits the production of estrogens, leading to a decrease in estrogen - mediated negative feedback of GnRH in the hypothalamus, which then stimulates the release of LH from the anterior pituitary . However another theory of the LH peak is a positive feedback mechanism from estradiol . The levels keep rising through the follicular phase and when they reach an unknown threshold, this results in the peak of the LH . This effect is opposite from the usual negative feedback mechanism presented at lower levels . In other words, the mechanism (s) are not yet clear . The increase in LH production only lasts for 24 to 48 hours . This "LH surge" triggers ovulation, thereby not only releasing the egg from the follicle, but also initiating the conversion of the residual follicle into a corpus luteum that, in turn, produces progesterone to prepare the endometrium for a possible implantation . LH is necessary to maintain luteal function for the second two weeks of the menstrual cycle . If pregnancy occurs, LH levels will decrease, and luteal function will instead be maintained by the action of hCG (human chorionic gonadotropin), a hormone very similar to LH but secreted from the new placenta . </P> <P> Gonadal steroids (estrogens and androgens) generally have negative feedback effects on GnRH - 1 release at the level of the hypothalamus and at the gonadotropes, reducing their sensitivity to GnRH . Positive feedback by estrogens also occurs in the gonadal axis of female mammals and is responsible for the midcycle surge of LH that stimulates ovulation . Although estrogens inhibit kisspeptin (Kp) release from kiss1 neurons in the ARC, estrogens stimulate Kp release from the Kp neurons in the AVPV . As estrogens' levels gradually increase the positive effect predominates, leading to the LH surge . GABA - secreting neurons that innervate GnRH - 1 neurons also can stimulate GnRH - 1 release . These GABA neurons also possess ERs and may be responsible for the GnRH - 1 surge . Part of the inhibitory action of endorphins on GnRH - 1 release is through inhibition of these GABA neurons . Rupture of the ovarian follicle at ovulation causes a drastic reduction in estrogen synthesis and a marked increase in secretion of progesterone by the corpus luteum in the ovary, reinstating a predominantly negative feedback on hypothalamic secretion of GnRH - 1 . </P>

What does lh do in the menstrual cycle
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