Gonadotropinfrigivelse

Gonadotropinfrigivelse, or gonadotropin release, refers to the secretion of the anterior pituitary gonadotropins—luteinizing hormone (LH) and follicle-stimulating hormone (FSH)—in response to gonadotropin-releasing hormone (GnRH) from the hypothalamus. The process is essential for regulating gonadal function and gametogenesis in both sexes.

GnRH is released from hypothalamic neurons in pulsatile bursts and travels to the anterior pituitary via the hypophyseal portal circulation. The GnRH pulses stimulate gonadotrophs to synthesize and secrete LH and FSH in a coordinated, but often pulsatile, manner. The pattern of GnRH secretion influences the relative release of LH and FSH: high-frequency pulses favor LH, while lower-frequency pulses favor FSH. The synthesis of the gonadotropin subunits and their release are also modulated by other hypothalamic factors and by feedback from the gonads.

Feedback regulation involves sex steroids and gonadal peptides. Estrogen, testosterone, and progesterone provide negative feedback to the hypothalamus and pituitary, shaping GnRH and gonadotropin secretion across the menstrual–ovarian and testicular–hormonal axes. Inhibins, produced by the gonads, specifically regulate FSH levels, while activins and follistatins modulate FSH synthesis and release.

Clinically, impaired or dysregulated gonadotropinfrigivelse underlies conditions such as central (hypothalamic) precocious puberty, hypogonadotropic hypogonadism, and certain pituitary disorders. Therapeutically, modulation of GnRH signaling—using GnRH agonists or antagonists—can either stimulate (via pulsatile GnRH administration) or suppress (via continuous administration) gonadotropin release, with applications in fertility treatment, puberty disorders, and hormone-dependent diseases.