Abstract

Reproductive function is controlled by the pituitary glycoproteins, luteinizing hormone (LH) and follicle stimulating hormone (FSH). The two hormones are composed of a common α-subunit and distinct β-subunits (1, 2). LH and FSH are secreted by the same pituitary gonadotrope cells, and their synthesis and secretion is controlled by the hypothalamic decapeptide gonadotropin releasing hormone (GnRH). GnRH is secreted into the hypophysial-portal blood in an intermittent manner (3, 4), and this pulsatile secretion is essential for maintaining gonadotropin synthesis and release (5–7). The pattern of pulsatile GnRH secretion changes in various physiologic circumstances (8, 9), and differential secretion of LH and FSH also occurs. Thus, it appears that a single gonadotropin releasing hormone can effect differential secretion of LH and FSH by the pituitary gonadotrope cell. Gonadal steroids can alter the pattern of GnRH secretion and also modify gonadotrope responses to GnRH Inhibin, a gonadal polypeptide, acts directly on the pituitary to selectively inhibit FSH secretion. Other gonadal peptides, such as activin, may also be involved in modifying gonadotrope responses to GnRH. Thus, the differential regulation of LH and FSH synthesis and secretion appears to result from changes in the pattern of the GnRH stimulus together with the direct feedback effects of gonadal steroids and peptides on the gonadotrope.

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