Nonhuman primates contribute unique understanding to anovulatory infertility in women

• Published in: ILAR journal Vol. 45; no. 2; pp. 116 - 131
• Main Authors: Abbott, D.H, Foong, S.C, Barnett, D.K, Dumesic, D.A
• Format: Journal Article
• Language: English
• Published: England Institute for Laboratory Animal Research 2004
• Subjects: animal models; Animals; anovulation; Anovulation - physiopathology; Disease Models, Animal; Female; female fertility; Gonadotropin-Releasing Hormone - metabolism; human health; Humans; Hyperprolactinemia - physiopathology; Hypothalamus - physiopathology; Infertility, Female - physiopathology; laboratory animals; Leptin - metabolism; literature reviews; monkeys; Ovarian Diseases - physiopathology; Primates - metabolism; Primates - physiology; Stress, Physiological - physiopathology; Time Factors; rhesus monkey; gonadotropin-releasing hormone; follicle-stimulating hormone; anovulation; marmoset; luteinizing hormone; hypothalamic amenorrhea; polycystic ovary syndrome
• ISSN: 1084-2020; 1930-6180
• DOI: 10.1093/ilar.45.2.116

Anovulatory infertility affects a large proportion of reproductive-aged women. Major improvements in successful clinical treatment of this prevalent disorder in women's health have been made possible because of biomedical research employing nonhuman primates. Experiments on female rhesus monkeys were the first to demonstrate that the key hypothalamic neurotransmitter, gonadotropin-releasing hormone, involved in stimulating pituitary gonadotropin synthesis, storage, and release was bioactive only when released in approximately hourly bursts. This breakthrough in understanding gonadotropin regulation enabled identification of hypogonadotropic, apparently normogonadotropic, and hypergonadotropic forms of anovulatory infertility, and development of appropriate stimulatory or inhibitory gonadotropin therapies. Treatments to overcome anovulatory infertility represent one of the major advances in clinical reproductive endocrinology during the last 25 yr. The future promise of nonhuman primate models for human ovulatory dysfunction, however, may be based on an increased understanding of molecular and physiological mechanisms responsible for fetal programming of adult metabolic and reproductive defects and for obesity-related, hyperinsulinemic impairment of oocyte development.