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,
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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45 citations,
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131 citations,
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March 2019 in “Critical Reviews in Clinical Laboratory Sciences” The androgen receptor is a promising target for breast cancer treatment, especially in triple-negative cases, but more research is needed for personalized therapies.
16 citations,
September 2008 in “Dermatologic Therapy” CAH is a genetic disorder affecting cortisol production and causing hormonal imbalances, with treatment and diagnosis varying by form and symptoms.
