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X-Inactivation

X-Inactivation

The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.

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Related Experiment Video

Updated: Jan 11, 2026

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome

Published on: October 2, 2018

Female Mice with HSD17B1 Inactivation Show Mild Hyperandrogenism without Notable Impact on Reproductive Function or

Arttu Junnila¹, Nataliia Petruk¹, Hanna Heikelä¹

¹Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku FI-20520, Finland.

|November 11, 2025

Summary

17β-hydroxysteroid dehydrogenase 1 (HSD17B1) enzyme activity was blocked in mice, leading to mild ovarian imbalances but no significant reproductive or bone health issues. The body compensated for the lack of estradiol production.

Keywords:

HSD17B1 bone health estrogens female reproduction hyperandrogenism steroidogenesis

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Published on: August 13, 2019

Area of Science:

Endocrinology
Molecular Biology
Reproductive Science

Background:

17β-hydroxysteroid dehydrogenase 1 (HSD17B1) activates estrone (E1) to estradiol (E2).
Species-specific differences in HSD17B1 activity exist, influenced by key amino acid substitutions like His222 in humans versus glycine in mice.

Purpose of the Study:

To investigate the functional consequences of HSD17B1 inactivation on estrogen metabolism and reproductive health in vivo.
To identify the role of HSD17B1 in regulating intraovarian and circulating steroid hormone levels.

Main Methods:

Molecular modeling to identify key amino acid differences in HSD17B1 between species.
Generation of HSD17B1 Ser143Ala knock-in (HSD17B1-KI) mice to block E1 to E2 conversion.
Analysis of ovarian and circulating hormone levels (E1, E2, androgens), LH, ovarian weight, fertility, gene expression, and tissue phenotypes.

Main Results:

HSD17B1 Ser143Ala mutation abolished E1 to E2 conversion, elevating E1 and androgens in HSD17B1-KI mice ovaries and circulation.
Despite hormonal imbalances, HSD17B1 inactivation had mild effects on female reproductive development and function, with no significant impact on fertility or extra-gonadal tissues.
Upregulation of genes related to steroidogenesis and PCOS markers observed in HSD17B1-KI ovaries.

Conclusions:

Mouse HSD17B1 activity blockade is compensated in vivo, causing only minor ovarian estrogen and androgen imbalances.
HSD17B1 plays a role in ovarian steroid homeostasis, but its inactivation does not lead to severe reproductive or bone health consequences in mice.
The study highlights the adaptability of the female reproductive system to altered estrogen synthesis pathways.