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Review
. 2018:107:377-422.
doi: 10.1016/bs.vh.2018.01.017. Epub 2018 Feb 22.

Developmental Programming of Ovarian Functions and Dysfunctions

Muraly Puttabyatappa  1 , Vasantha Padmanabhan  2
Affiliations
Review

Developmental Programming of Ovarian Functions and Dysfunctions

Muraly Puttabyatappa et al. Vitam Horm. 2018.

Abstract

The pathophysiological mechanisms underlying the origin of several ovarian pathologies remain unclear. In addition to the genetic basis, developmental insults are gaining attention as a basis for the origin of these pathologies. Such early insults include maternal over or under nutrition, stress, and exposure to environmental chemicals. This chapter reviews the development and physiological function of the ovary, the known ovarian pathologies, the developmental check points of ovarian differentiation impacted by developmental insults, the role played by steroidal and metabolic factors as mediaries, the epigenetic mechanisms via which these mediaries induce their effects, and the knowledge gaps for targeting future studies to ultimately aid in the development of improved treatments.

Keywords: Androgens; DOHAD; Estrogens; Female reproduction; Granulosa cells; Hyperandrogenism; Insulin; Ovary; Polycystic ovary syndrome; Theca cells.

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Figures

Figure 1:
Figure 1:
Schematic showing the different stages of follicular differentiation and the developmental checkpoints, potential targets for developmental insults.
Figure 2:
Figure 2:
Fetal and adult ovarian changes that account for enhanced follicular recruitment and follicular persistence evidenced in prenatal T-treated sheep. Increases in gene / protein markers are denoted in green and decreases in orange.
See this image and copyright information in PMC

References

    1. Abbott DH, Barnett DK, Bruns CM & Dumesic DA 2005. Androgen excess fetal programming of female reproduction: a developmental aetiology for polycystic ovary syndrome? Hum Reprod Update 11 357–374. - PubMed
    1. Abbott DH, Barnett DK, Levine JE, Padmanabhan V, Dumesic DA, Jacoris S, and Tarantal AF 2008. Endocrine antecedents of polycystic ovary syndrome in fetal and infant prenatally androgenized female rhesus monkeys. Biol Reprod 79 154–163. - PMC - PubMed
    1. Abi Salloum B, Veiga-Lopez A, Abbott DH, Burant CF, and Padmanabhan V 2015. Developmental programming: exposure to testosterone excess disrupts steroidal and metabolic environment in pregnant sheep. Endocrinology 156 2323–2337. - PMC - PubMed
    1. Adewale HB, Jefferson WN, Newbold RR, and Patisaul HB 2009. Neonatal bisphenol-a exposure alters rat reproductive development and ovarian morphology without impairing activation of gonadotropin-releasing hormone neurons. Biol Reprod 81 690–699. - PMC - PubMed
    1. Alexanderson C, Eriksson E, Stener-Victorin E, Lystig T, Gabrielsson B, Lonn M & Holmang A 2007. Postnatal testosterone exposure results in insulin resistance, enlarged mesenteric adipocytes, and an atherogenic lipid profile in adult female rats: comparisons with estradiol and dihydrotestosterone. Endocrinology 148 5369–5376. - PubMed

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