Gonadotropin-‐Releasing Hormone

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Gonadotropin-Releasing Hormone By Ronald Steriti, ND, PhD © 2011 Gonadotropin-releasing hormone (GnRH), also known as Luteinizing- hormone-releasing hormone (LHRH) and luliberin, is a tropic peptide hormone responsible for the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary. GnRH is synthesized and released from neurons within the hypothalamus. GnRH activity is very low during childhood, and is activated at puberty. During the reproductive years, pulse activity is critical for successful reproductive function as controlled by feedback loops. However, once a pregnancy is established, GnRH activity is not required. Pulsatile activity can be disrupted by hypothalamic-pituitary disease, either dysfunction (i.e., hypothalamic suppression) or organic lesions (trauma, tumor). In normal females, GnRH secretion is regulated by estradiol and progesterone. (Evans, Richter et al. 2002) (Sun and Moenter 2010) Elevated prolactin levels decrease GnRH activity. (Page-Wilson, Smith et al. 2006) (Koike, Miyake et al. 1991) In contrast, hyperinsulinemia increases pulse activity leading to disorderly LH and FSH activity, as seen in polycystic ovary syndrome (PCOS). (Patel, Coffler et al. 2004) GnRH Agonists GnRH agonist drugs are used to suppress ovarian activity and induce a hypo-estrogenic state. They are uses in patients with prostate and breast cancer. Kallmann Syndrome GnRH formation is congenitally absent in Kallmann syndrome. Adiposogenital Dystrophy Adiposogenital dystrophy is a condition which may be caused by secondary hypogonadism originating from decreased levels in GnRH. Low levels of GnRH has been associated with defects of the feeding centers of the hypothalamus, leading to an increase consumption of food and thus caloric intake. It is characterized by: Feminine obesity Growth retardation and retarded sexual development, atrophy or hypoplasia of the gonads, and altered secondary sex characteristics, Headaches mental retardation, problems with vision polyuria, polydipsia. References Evans, N. P., T. A. Richter, et al. (2002). "Neuroendocrine mechanisms underlying the effects of progesterone on the oestradiol-induced GnRH/LH surge." Reprod Suppl 59: 57-66. Koike, K., A. Miyake, et al. (1991). "Effect of prolactin on the secretion of hypothalamic GnRH and pituitary gonadotropins." Horm Res 35 Suppl 1: 5-12. Page-Wilson, G., P. C. Smith, et al. (2006). "Prolactin suppresses GnRH but not TSH secretion." Horm Res 65(1): 31-8. Patel, K., M. S. Coffler, et al. (2004). "Relationship of GnRH-stimulated LH release to episodic LH secretion and baseline endocrine-metabolic measures in women with polycystic ovary syndrome." Clin Endocrinol (Oxf) 60(1): 67-74. Sun, J. and S. M. Moenter (2010). "Progesterone treatment inhibits and dihydrotestosterone (DHT) treatment potentiates voltage-gated calcium currents in gonadotropin-releasing hormone (GnRH) neurons." Endocrinology 151(11): 5349-58. .

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