Abstract
Several studies have attempted to explain the high overall prevalence of polycystic ovary syndrome among women worldwide (about 4-10%) despite its link to subfertile phenotypes. For this reason, it is considered an evolutionary paradox. In this review, we show that several genetic loci associated with the disease differently modulate the reproductive parameters of men and women. This observation suggests that such genetic variants lead to opposite effects in the two sexes in reproductive success. Intralocus sexual conflict as a cause of the persistence polycystic ovary syndrome genotypes among humans is supported.
Keywords:
PCOS; evolution; gender; hyperandrogenic; metabolic; sex-specific.
Copyright © 2016 Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Antigens, CD / genetics
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Death Domain Receptor Signaling Adaptor Proteins / genetics
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Evolution, Molecular
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Female
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Genes, X-Linked
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Genetic Drift
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Guanine Nucleotide Exchange Factors / genetics
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Humans
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Infertility / genetics
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Male
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Metabolic Diseases / complications
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Metabolic Diseases / genetics
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Metabolic Diseases / metabolism
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Neoplasm Proteins / genetics
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Phosphoproteins / genetics
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Polycystic Ovary Syndrome / complications
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Polycystic Ovary Syndrome / epidemiology
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Polycystic Ovary Syndrome / genetics*
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Receptor, Insulin / genetics
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Receptors, FSH / genetics
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Receptors, LH / genetics
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Transcription Factors
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YAP-Signaling Proteins
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rab5 GTP-Binding Proteins / genetics
Substances
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Adaptor Proteins, Signal Transducing
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Antigens, CD
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DENND1A protein, human
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Death Domain Receptor Signaling Adaptor Proteins
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Guanine Nucleotide Exchange Factors
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Neoplasm Proteins
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Phosphoproteins
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Receptors, FSH
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Receptors, LH
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THADA protein, human
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Transcription Factors
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YAP-Signaling Proteins
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YAP1 protein, human
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INSR protein, human
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Receptor, Insulin
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RAB5C protein, human
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rab5 GTP-Binding Proteins