Part of “CHAPTER 95 – THE NORMAL MENSTRUAL CYCLE AND THE CONTROL OF OVULATION“

In most respects, the events of the luteal phase are consequences of preceding follicular phase activities. Indeed, the process of luteinization begins even before the time of ovulation (see Chap. 94). The granulosa and theca cells that, together with the oocyte, form the dominant follicle and secrete large amounts of estrogens and regulatory peptides are transformed into the corpus luteum after ovulation. In the luteal phase, these same cells produce progesterone as their primary secretory product, but estrogens still are produced in large amounts as well. The synergism of high estrogen levels and FSH in the late follicular phase induces LH receptors on granulosa cells and leads to progesterone secretion even before the LH surge. This change in granulosa cell function is known as luteinization.111 It would seem, therefore, that the greater the proliferation of FSH-stimulated granulosa cells in the follicular phase, the greater will be the transformed luteinized cell mass for progesterone production and early pregnancy support.

Luteinization of granulosa and theca cells occurs only within the dominant follicle; nearby granulosa cells remain unaffected. Thus, intraovarian regulators have been suggested as important in causing this localized phenomenon as well. A luteinizing inhibitor is a convenient concept for explaining why other nearby ovarian cells do not undergo luteinization, especially because all granulosa cells removed from the ovary and cultured in vitro appear to luteinize spontaneously. Such a substance remains to be isolated and characterized.