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Which origin for polycystic ovaries syndrome: Genetic, environmental or both?

Abstract Polycystic ovaries syndrome (PCOS), the most common female endocrine disorder, affects 7-10% of women of childbearing age. It includes ovarian hyperandrogenism, impaired follicular maturation, anovulation and subfertility. Insulin resistance, although present in most cases, is not necessary for diagnosis. It increases hyperandrogenism and long-term metabolic, cardiovascular and oncological risks. The origin of hyperandrogenism and hyperinsulinemia has a genetic component, as demonstrated by familial aggregation studies and recent identification of associated genomic variants, conferring a particular susceptibility to the syndrome. However, experimental and epidemiological evidences also support a developmental origin via a deleterious foetal environment, concerning the endocrine status (foetal hyperandrogenism), the nutritional level (intrauterine growth retardation), or the toxicological exposure (endocrine disruptors). Epigenetic changes recently reported in the literature as associated with PCOS, enhance this hypothesis of foetal reprogramming of the future adult ovarian function by environmental factors. Better characterisation of these genetic, epigenetic, or environmental factors, could lead to earlier prevention and more efficient treatments.
PMID
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AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS, AMERICAN COLLEGE OF ENDOCRINOLOGY, AND ANDROGEN EXCESS AND PCOS SOCIETY DISEASE STATE CLINICAL REVIEW: GUIDE TO THE BEST PRACTICES IN THE EVALUATION AND TREATMENT OF POLYCYSTIC OVARY SYNDROME--PART 1.

Authors

Mayor MeshTerms
Keywords

Environmental endocrine disruptors

Epigenetics

Foetal programming

Genomic variant

Hyperandrogenism

Hyperandrogénie ovarienne

Insulin resistance

Insulino-résistance

Maturation folliculaire

Perturbateurs endocriniens environnementaux

Polycystic ovaries syndrome

Programmation fœtale

SOPK

Variant génétique

Épigénétique

Journal Title annales d'endocrinologie
Publication Year Start




PMID- 28606381
OWN - NLM
STAT- In-Process
DA  - 20170613
LR  - 20170710
IS  - 2213-3941 (Electronic)
IS  - 0003-4266 (Linking)
VI  - 78
IP  - 3
DP  - 2017 Jul
TI  - Which origin for polycystic ovaries syndrome: Genetic, environmental or both?
PG  - 176-185
LID - S0003-4266(17)30048-3 [pii]
LID - 10.1016/j.ando.2017.04.024 [doi]
AB  - Polycystic ovaries syndrome (PCOS), the most common female endocrine disorder,
      affects 7-10% of women of childbearing age. It includes ovarian hyperandrogenism,
      impaired follicular maturation, anovulation and subfertility. Insulin resistance,
      although present in most cases, is not necessary for diagnosis. It increases
      hyperandrogenism and long-term metabolic, cardiovascular and oncological risks.
      The origin of hyperandrogenism and hyperinsulinemia has a genetic component, as
      demonstrated by familial aggregation studies and recent identification of
      associated genomic variants, conferring a particular susceptibility to the
      syndrome. However, experimental and epidemiological evidences also support a
      developmental origin via a deleterious foetal environment, concerning the
      endocrine status (foetal hyperandrogenism), the nutritional level (intrauterine
      growth retardation), or the toxicological exposure (endocrine disruptors).
      Epigenetic changes recently reported in the literature as associated with PCOS,
      enhance this hypothesis of foetal reprogramming of the future adult ovarian
      function by environmental factors. Better characterisation of these genetic,
      epigenetic, or environmental factors, could lead to earlier prevention and more
      efficient treatments.
CI  - Copyright (c) 2017 Elsevier Masson SAS. All rights reserved.
FAU - Fenichel, Patrick
AU  - Fenichel P
AD  - Department of Endocrinology, Diabetology and Reproduction, groupe hospitalier
      l'Archet, CHU de Nice, 151, route de Saint-Antoine-de-Ginestiere, 06202 Nice,
      France; Inserm U1065/C3M, hopital de l'Archet, 151, route de
      Saint-Antoine-de-Ginestiere, 06202 Nice, France. Electronic address:
      [email protected]
FAU - Rougier, Charlotte
AU  - Rougier C
AD  - Department of Endocrinology, Diabetology and Reproduction, groupe hospitalier
      l'Archet, CHU de Nice, 151, route de Saint-Antoine-de-Ginestiere, 06202 Nice,
      France.
FAU - Hieronimus, Sylvie
AU  - Hieronimus S
AD  - Department of Endocrinology, Diabetology and Reproduction, groupe hospitalier
      l'Archet, CHU de Nice, 151, route de Saint-Antoine-de-Ginestiere, 06202 Nice,
      France.
FAU - Chevalier, Nicolas
AU  - Chevalier N
AD  - Department of Endocrinology, Diabetology and Reproduction, groupe hospitalier
      l'Archet, CHU de Nice, 151, route de Saint-Antoine-de-Ginestiere, 06202 Nice,
      France; Inserm U1065/C3M, hopital de l'Archet, 151, route de
      Saint-Antoine-de-Ginestiere, 06202 Nice, France.
LA  - eng
PT  - Journal Article
DEP - 20170609
PL  - France
TA  - Ann Endocrinol (Paris)
JT  - Annales d'endocrinologie
JID - 0116744
OTO - NOTNLM
OT  - Environmental endocrine disruptors
OT  - Epigenetics
OT  - Foetal programming
OT  - Genomic variant
OT  - Hyperandrogenism
OT  - Hyperandrogenie ovarienne
OT  - Insulin resistance
OT  - Insulino-resistance
OT  - Maturation folliculaire
OT  - Perturbateurs endocriniens environnementaux
OT  - Polycystic ovaries syndrome
OT  - Programmation foetale
OT  - SOPK
OT  - Variant genetique
OT  - Epigenetique
EDAT- 2017/06/14 06:00
MHDA- 2017/06/14 06:00
CRDT- 2017/06/14 06:00
PHST- 2017/02/24 [received]
PHST- 2017/04/20 [revised]
PHST- 2017/04/26 [accepted]
AID - S0003-4266(17)30048-3 [pii]
AID - 10.1016/j.ando.2017.04.024 [doi]
PST - ppublish
SO  - Ann Endocrinol (Paris). 2017 Jul;78(3):176-185. doi: 10.1016/j.ando.2017.04.024. 
      Epub 2017 Jun 9.