At present, 14 different types of the hydroxysteroid (17-beta) dehydrogenase (HSD17B) enzymes have been characterized. These enzymes differ from each other according to tissue distribution, substrate specificity, subcellular localization and expression regulation. In this study, the main focus was to characterize the physiological function of one member of the enzyme superfamily, namely, hydroxysteroid (17-beta) dehydrogenase 12 (HSD17B12). HSD17B12 is widely expressed in different human tissues and has been suggested to function in fatty acid elongation as well as in sex steroid metabolism. However, the main function of HSD17B12 in vivo is still poorly understood. 

The main aim of this study was to characterize the role of HSD17B12 in the ovarian physiology and fetal development. The HSD17B12 enzyme has a similar tissue distribution in mice and humans, and therefore, the HSD17B12 knockout mouse model was used to provide information about its role in humans. Furthermore, the expression of HSD17B12 enzyme was studied in different human epithelial ovarian cancer types. 

According to our study, absence of the enzyme causes embryonic lethality, and even the loss of one allele leads to ovarian dysfunction and fertility problems in mice. Furthermore, we found that the expression of the HSD17B12 enzyme positively correlates with the grade of human ovarian cancer. However, the role of the enzyme in cancer progression is still poorly understood, necessitating further studies. In conclusion, our study indicates that the HSD17B12 enzyme is necessary for embryonal development and female fertility; however, its overexpression may play a role in ovarian cancer development and/or progression.