New Insights Into Testosterone Biosynthesis: Novel Observations From HSD17B3 Deficient Mice

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.