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Published on: July 14, 2016
Human HSD17B1 expression masculinizes transgenic female mice
Taija Saloniemi1, Michelle Welsh, Tarja Lamminen
1Department of Physiology, Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, FI-20014 Turku, Finland. taija.saloniemi@utu.fi
Molecular and Cellular Endocrinology
|December 9, 2008
Summary
Excess androgens during fetal development cause female masculinization. Overexpression of human hydroxysteroid 17-beta dehydrogenase 1 (HSD17B1) in mice led to masculinized female traits, suggesting a role in hormonal imbalances.
Area of Science:
- Endocrinology
- Developmental Biology
- Molecular Endocrinology
Background:
- Excess fetal androgens can disrupt normal female development, leading to masculinization.
- Hydroxysteroid (17beta) dehydrogenases (HSD17Bs) are key enzymes regulating steroid hormone concentrations.
- Human HSD17B1 converts estrone to estradiol and androstenedione to testosterone.
Purpose of the Study:
- To investigate the role of human HSD17B1 in fetal development and potential contribution to female masculinization.
- To further characterize the effects of HSD17B1 overexpression on female reproductive tract development in a mouse model.
Main Methods:
- Utilized transgenic mice overexpressing human HSD17B1.
- Examined the reproductive anatomy of HSD17B1-overexpressing female mice.
- Analyzed the expression of HSD17B1 in fetal human ovaries.
Main Results:
- HSD17B1 overexpression in female mice resulted in masculinized phenotypes.
- These females exhibited internal structures resembling Wolffian ducts and an enlarged Skene paraurethral gland (female prostate).
- HSD17B1 is expressed in the fetal human ovary.
Conclusions:
- Abnormal fetal expression of HSD17B1 may contribute to hormonal imbalances and female masculinization.
- HSD17B1 plays a role in normal steroid hormone regulation during development.
- Targeting HSD17B1 could be relevant for understanding and potentially treating conditions associated with hormonal imbalances.
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