TLDR Mice without the enzyme HSD17B3 still produce normal testosterone, suggesting they have different ways to make it compared to humans.
The study on HSD17B3 deficient mice reveals that despite the deficiency, these mice maintain testosterone production, masculinization, and fertility, unlike humans with HSD17B3 mutations who experience disorders of sexual development due to low testosterone levels. The findings suggest alternative pathways and enzymes, such as HSD17B1, HSD17B5, and HSD17B12, may compensate for the loss of HSD17B3 in mice, highlighting species differences in androgen production. This research underscores the complexity of testosterone biosynthesis and suggests potential targets for novel therapies to regulate testosterone in individuals with deficiencies.
35 citations
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May 2022 in “Baillière's best practice and research in clinical endocrinology and metabolism/Baillière's best practice & research. Clinical endocrinology & metabolism” Androgens like testosterone are important hormones for both men and women, made differently in each sex and affecting the body by regulating genes and quick interactions with cell components.
70 citations
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131 citations
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September 2017 in “Molecular and Cellular Endocrinology” The document concludes that blocking the internal pathways that create androgens might help treat cancers that depend on sex hormones.
157 citations
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May 2021 in “Endocrine Reviews” Early diagnosis and individualized treatment improve outcomes for Congenital Adrenal Hyperplasia.
December 2015 in “University of Birmingham Institutional Research Archive (University of Birmingham)” AKR1C3 could be a treatment target for metabolic issues in PCOS.
