The physiology and pathophysiology of inhibin, activin and follistatin in female reproduction.
In the last 2 years, major advances have been made in the understanding of inhibin physiology. Discovery of an inhibin receptor and binding protein has expanded our knowledge of the mechanism whereby inhibin antagonizes activin action. Controlled experimental studies have clarified the regulation and physiology of inhibin A and inhibin B, providing evidence for their use as markers of ovarian function. Clinical studies continue to uphold the use of inhibin as a marker for ovarian cancer, but have not generally supported its use over standard prognostic markers in assisted reproductive technologies. Finally, ongoing work suggests alterations in inhibin and follistatin that may be linked to the pathophysiology of polycystic ovary syndrome. Thus, the mechanism of inhibin action and its role in normal and abnormal ovarian function continues to emerge.
Welt
Corrine K
CK
Reproductive Endocrine Unit, Reproductive Endocrine Sciences Center and National Center for Infertility Research, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. cwelt@partners.org
D028341:Activins / Q000096:biosynthesis; D005260:Female; D005298:Fertility / Q000502:physiology*; D038681:Follistatin; D006801:Humans; D007247:Infertility, Female / Q000503:physiopathology*; D007265:Inhibins / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D011085:Polycystic Ovary Syndrome / Q000503:physiopathology; D011247:Pregnancy
D038681:Follistatin; D028341:Activins; D007265:Inhibins