Endocrine luteotropins are produced at a distance from their target organ, the corpus luteum. They include:  hCG, a 37-kilodalton glycoprotein secreted by the trophoblast of the chorion, which stimulates LH receptors on the corpus luteum and prevents its degeneration (page 840)  LH and prolactin, both secreted by the pituitary gland  Insulin, produced by the pancreas
High levels of progesterone, produced from cholesterol by the corpus luteum, block the cyclic development of ovarian follicles. In early pregnancy, the corpus luteum measures 2 cm to 3 cm, thus filling most of the ovary. Its function begins to decline gradually after 8 weeks of pregnancy, although it persists throughout pregnancy. Although the corpus luteum remains active, the placenta produces sufficient amounts of estrogens and progestogens from maternal and fetal precursors to take over the function of the corpus luteum after 6 weeks of pregnancy. Human chorionic gonadotropin (hCG) can be detected in the serum as early as 6 days after conception and in the urine as early as 10 to 14 days of pregnancy. Detection of hCG in the urine by specific antibodies forms the basis of most over-the-counter pregnancy tests. In addition, the rapid increase in circulating level of hGC in early pregnancy is responsible for “morning sickness,” a condition characterized by nausea and vomiting. These symptoms usually occur in the early hours of the morning are often among the first signs of pregnancy.
Most ovarian follicles are lost by atresia mediated by apoptosis of granulosa cells.
As stated, very few of the ovarian follicles that begin their differentiation in the embryonic ovary are destined to complete their maturation. Most of the follicles degenerate and disappear through a process called ovarian follicular atresia. Atresia is mediated by apoptosis of granulosa cells. Large numbers of follicles undergo atresia during fetal development, early postnatal life, and puberty. After puberty, groups of follicles begin to mature during each menstrual cycle; normally, only one follicle completes its maturation. Atresia is now thought to be a mechanism whereby a few follicles are stimulated to maintain their development through the programmed death of the other follicles. Thus, at any stage of its maturation a follicle may undergo atresia. The process becomes more complex as the follicle progresses toward maturation.
In atresia of primordial and small, growing follicles, the immature oocyte becomes smaller and degenerates; similar changes occur in the granulosa cells. Atretic follicles shrink and eventually disappear from the stroma of the ovary as a result of repeated apoptosis and phagocytosis by granulosa cells (Plate 93, page 874). As the cells are reabsorbed and disappear, the surrounding stromal cells migrate into the space previously occupied by the follicle, leaving no trace of its existence.