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Review
. 2016 Jul 16;14(1):38.
doi: 10.1186/s12958-016-0173-x.

Genetic, hormonal and metabolic aspects of PCOS: an update

Affiliations
Review

Genetic, hormonal and metabolic aspects of PCOS: an update

V De Leo et al. Reprod Biol Endocrinol. .

Abstract

Polycystic ovary syndrome (PCOS) is a complex endocrine disorder affecting 5-10 % of women of reproductive age. It generally manifests with oligo/anovulatory cycles, hirsutism and polycystic ovaries, together with a considerable prevalence of insulin resistance. Although the aetiology of the syndrome is not completely understood yet, PCOS is considered a multifactorial disorder with various genetic, endocrine and environmental abnormalities. Moreover, PCOS patients have a higher risk of metabolic and cardiovascular diseases and their related morbidity, if compared to the general population.

Keywords: Genetic; Hyperandrogenism; Infertility; Insulin-resistance; Metformin; Myo-inositol; Oral contraceptives; PCOS.

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Figures

Fig. 1
Fig. 1
Theory of prenatal origin of PCOS and its development at puberty
Fig. 2
Fig. 2
Alteration of extra- and intra-ovarian factors may compromise follicular development and oocyte development in PCOS
Fig. 3
Fig. 3
In a normal cycle, only the dominant follicle responds to LH when it reaches 10 mm diameter. In PCOS the response to LH occurs inappropriately in smaller follicles and many antral follicles reach terminal differentiation before time, producing a greater quantity of steroids and inhibin B that exert negative feedback on FSH production
Fig. 4
Fig. 4
Relative inhibition of 17–20 lyase activity with respect to 17-hydroxylase has been found in women with PCOS. This leads to an increase in the 17OHP/A ratio and reduction of aromatase activity, the enzyme of granulosa cells that converts androgens into estrogens
Fig. 5
Fig. 5
Hyperinsulinemia stimulates directly cytochrome p450 enzymes in the ovary or indirectly through action of LH or IGF-1, causing hyperandrogenism
Fig. 6
Fig. 6
Insulin resistance is the link between PCOS and metabolic syndrome
Fig. 7
Fig. 7
Factors involved in the etiopathogenesis of miscarriage in women with PCOS

References

    1. The Rotterdam ESHRE/ASRM-sponsored PCOS consensus workshop group Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS) Hum Reprod. 2004;19:41–47. doi: 10.1093/humrep/deh098. - DOI - PubMed
    1. Zawadski JK, Dunaif A. Diagnostic criteria for polycystic ovary syndrome: towards a rational approach. In: Dunaif A, Givens JR, Haseltine F, editors. Polycystic ovary syndrome. Boston: Blackwell Scientific; 1992. pp. 377–384.
    1. Azziz R, Carmina E, Dewailly D, et al. Criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: An Androgen Excess guideline. J Clin Endocrinol Metab. 2006;91:4237–4245. doi: 10.1210/jc.2006-0178. - DOI - PubMed
    1. Franks S, Mc Carthy M, Hardy K. Development of polycystic ovary syndrome: involvement of genetic and environmental factors. Int J Androl. 2006;29:278–285. doi: 10.1111/j.1365-2605.2005.00623.x. - DOI - PubMed
    1. De Leo V, La Marca A. Petraglia F Insulin-lowering agents in the management of polycystic ovary syndrome. Endocr Rev. 2003;24:633–667. doi: 10.1210/er.2002-0015. - DOI - PubMed

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