Hydroxysteroid (17β) dehydrogenase 13 deficiency triggers hepatic steatosis and inflammation in mice

What is it about?

Hydroxysteroid (17beta) dehydrogenases (HSD17Bs) form an enzyme family characterized by their ability to catalyze reactions in steroid and lipid metabolism. In the present study, we characterized the mouse strain in which the Hsd17b13 gene was disrupted. This resulted to fat accumulation in the liver cells of the mutant mice, indicated by observed increase in the size of the lipid droplets in the liver cells and by the increased concentration of triglycerides and certain lipid metabolites in the liver. These metabolic changes were associated with alterations in the appearance of key proteins in fatty acid metabolism. The pathophysiology observed mimics key features of non-alcoholic fatty liver disease in humans. Our data indicate that disruption of Hsd17b13 impairs hepatic lipid metabolism in mice, resulting the in fat accumulation and inflammation in the liver, while the enzyme does not play a major role in the regulation of reproductive functions. To further assess the functional relevance of HDS17B13 alterations for the development of fatty liver disease in human require additional studies.

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