Abbott publishes review on origins of PCOS in Reproduction

David Abbott, PhD, professor in the Division of Reproductive Sciences, co-authored a new publication published in Reproduction. Co-authors include Jon Levine, PhD; Phillip Dumesic, MD, PhD; Vasantha Padmanabhan, MS, PhD; and Daniel Dumesic, MD.

In “Origins and Implications: Gestational anti-Müllerian hormone and testosterone excess combined with maternal adiposity program for polycystic ovary syndrome”, Abbott and co-authors propose a unifying hypothesis on the origins of polycystic ovary syndrome (PCOS), combining high anti-Müllerian hormone, testosterone and obesity in the developmental origins and amplification of genetic variants predisposing to PCOS. The authors suggest: 

“Evidence is accumulating for fetal extra-ovarian production and action of AMH in various tissues: the brain, for survival of GnRH neurons migrating from the embryonic nose to the hypothalamus; the pituitary, for gonadotrope development; and the placenta, for optimal fetal support. In addition, PCOS risk genes, including those regulating androgen biosynthesis, are being identified in many families with PCOS, bestowing the potential for intrinsic androgen excess in the fetal ovary, adrenal, brain, abdominal adipose and pilosebaceous glands. A ‘two hit’ developmental origin may therefore promote PCOS pathogenesis during gestation when epigenetic mechanisms amplify genetically heritable traits, while accompanying metabolic perturbations, including gestational hyperglycemia, hypertension and maternal obesity, may exaggerate the phenotypic expression of PCOS.”

Read the whole study here!

**by Ob-Gyn Communications Intern Melis Baskaya