Abstract
AbstractAs a common endocrinopathy of reproductive-aged women, polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism, oligo-anovulation and polycystic ovarian morphology. It is linked with insulin resistance through preferential abdominal fat accumulation that is worsened by obesity. Over the past two millennia, menstrual irregularity, male-type habitus and sub-infertility have been described in women and confirm that these clinical features of PCOS were common in antiquity. Recent findings in normal-weight hyperandrogenic PCOS women show that exaggerated lipid accumulation by subcutaneous (SC) abdominal stem cells during development to adipocytes in vitro occurs in combination with reduced insulin sensitivity and preferential accumulation of highly-lipolytic intra-abdominal fat in vivo. This PCOS phenotype may be an evolutionary metabolic adaptation to balance energy storage with glucose availability and fatty acid oxidation for optimal energy use during reproduction. This review integrates fundamental endocrine-metabolic changes in healthy, normal-weight PCOS women with similar PCOS-like traits present in animal models in which tissue differentiation is completed during fetal life as in humans to support the evolutionary concept that PCOS has common ancestral and developmental origins.
Funder
Eunice Kennedy Shriver National Institute of Child Health and Human Development
National Center for Advancing Translational Sciences
Oregon National Primate Research Center
National Institute of Diabetes and Digestive and Kidney Diseases
Wisconsin National Primate Research Center
Santa Monica Bay Woman’s Club
Publisher
Springer Science and Business Media LLC
Subject
Developmental Biology,Endocrinology,Reproductive Medicine,Obstetrics and Gynecology
Reference114 articles.
1. Chang RJ, Dumesic DA. Polycystic ovary syndrome and Hyperandrogenic states. In: Strauss III JF, Barbieri RL, editors. Yen and Jaffe’s reproductive endocrinology: physiology, pathophysiology and clinical management. 8th ed. Philadelphia: Elsevier Saunders; 2018. p. 520–55.
2. Dumesic DA, Oberfield SE, Stener-Victorin E, Marshall JC, Laven JS, Legro RS. Scientific statement on the diagnostic criteria, epidemiology, pathophysiology, and molecular genetics of polycystic ovary syndrome. Endocr Rev. 2015;36(5):487–525.
3. Moran LJ, Misso ML, Wild RA, Norman RJ. Impaired glucose tolerance, type 2 diabetes and metabolic syndrome in polycystic ovary syndrome: a systematic review and meta-analysis. Hum Repro Update. 2010;16(4):347–63.
4. Dumesic DA, Hoyos LR, Chazenbalk GD, Naik R, Padmanabhan V, Abbott DH. Mechanisms of intergenerational transmission of polycystic ovary syndrome. Reproduction. 2019;159(1):R1–R13.
5. Abbott DH, Dumesic DA. Levine JE Hyperandrogenic origins of polycystic ovary syndrome – implications for pathophysiology and therapy. Expert Rev Endocrinol Metab. 2019;14(2):131–43.
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