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Prenatal ethanol exposure induces susceptibility to premature ovarian insufficiency

Yuan Ni1, Dan Xu2, Feng Lv3

  • 1Y Ni, Reproductive Medicine Center, Wuhan University Renmin Hospital, Wuhan, China.

The Journal of Endocrinology
|July 26, 2019
PubMed

Insights

Prenatal ethanol exposure (PEE) increases premature ovarian insufficiency (POI) risk in female offspring. This occurs due to intrauterine programming, specifically over-activation of the ovarian insulin-like growth factor 1 (IGF1) pathway, leading to depleted primordial follicles.

Area of Science:

  • Reproductive Biology
  • Developmental Toxicology
  • Endocrinology

Background:

  • Prenatal ethanol exposure (PEE) is a known teratogen impacting fetal development.
  • The reproductive system is particularly vulnerable to adverse intrauterine environments.
  • Premature ovarian insufficiency (POI) is a condition characterized by early loss of ovarian function.

Purpose of the Study:

  • To investigate the long-term effects of PEE on female offspring reproductive capacity.
  • To confirm PEE-induced susceptibility to premature ovarian insufficiency (POI).
  • To elucidate the intrauterine programming mechanisms underlying PEE-induced POI.

Main Methods:

  • Wistar rats were exposed to ethanol during gestation (GD 9-20).
  • Offspring reproductive parameters were assessed at fetal, pubertal, and adult stages.
  • In vitro studies used human granulosa cells (KGN) treated with ethanol and IGF1 siRNA.

Main Results:

  • PEE fetuses exhibited reduced oocyte numbers, increased apoptosis, and upregulated ovarian IGF1 signaling and steroidogenic enzymes.
  • Adult female offspring showed increased follicular atresia, decreased antral follicles, lower estradiol (E2), and elevated follicle-stimulating hormone (FSH).
  • In vitro, ethanol increased IGF1 pathway components, steroidogenic enzymes (3β-HSD, P450arom), and E2 production in KGN cells, effects partially reversed by IGF1 siRNA.

Conclusions:

  • PEE induces susceptibility to POI in adult female offspring.
  • The mechanism involves intrauterine programming via over-activation of the fetal ovarian IGF1 signaling pathway and steroidogenesis.
  • This leads to accelerated folliculogenesis and premature depletion of primordial follicles, ultimately causing POI.

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