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Whereas the ovary produces the majority of estradiol (E 2 ) in mature female primates, extraovarian sources contribute to E 2  synthesis and action, including the brain E 2 -regulating hypothalamic gonadotropin-releasing hormone. In ovary-intact female rodent models, aromatase inhibition (AI) induces a polycystic ovary syndrome-like hypergonadotropic hyperandrogenism due to absent E 2 -mediated negative feedback. To examine the role of extraovarian E 2  on nonhuman primate gonadotropin regulation, the present study uses letrozole to elicit AI in adult female marmoset monkeys. Sixteen female marmosets ( Callithrix jacchus; &gt;2 yr) were randomly assigned to ovary-intact or ovariectomy (OVX) conditions and subsequently placed on a daily oral regimen of either ~200 µl vehicle alone (ovary-intact Control, n = 3; OVX, n = 3) or 1 mg ⋅ kg −1  ⋅ day −1  letrozole in vehicle (ovary-intact AI, n = 4; OVX + AI, n = 6). Blood samples were collected every 10 days, and plasma chorionic gonadotropin (CG) and steroid hormone levels were determined by validated radioimmunoassay and liquid chromatography/tandem mass spectrometry, respectively. Ovary-intact, AI-treated and OVX females exhibited elevated CG ( P &lt; 0.01, P = 0.004, respectively) compared with controls, and after 30 days, OVX + AI females exhibited a suprahypergonadotropic phenotype ( P = 0.004) compared with ovary-intact + AI and OVX females. Androstenedione ( P = 0.03) and testosterone ( P = 0.05) were also elevated in ovary-intact, AI-treated females above all other groups. The current study thus confirms in a nonhuman primate that E 2  depletion and diminished negative feedback in ovary-intact females engage hypergonadotropic hyperandrogenism. Additionally, we demonstrate that extraovarian estrogens, possibly neuroestrogens, contribute to female negative feedback regulation of gonadotropin release.

Extraovarian gonadotropin negative feedback revealed by aromatase inhibition in female marmoset monkeys