ECE2017 Eposter Presentations: Diabetes, Obesity and Metabolism Obesity (81 abstracts)
Hydroxysteroid (17beta) dehydrogenase 13 knockout mice present with inflammation associated liver steatosis
Hanna Heikelä 1 , Marion Adam 1 , Dorothea Portius 2 , Jenni Mäki-Jouppila 1 , Arfa Mehmood 1, , Prem Adhikari 1 , Irene Esposito 4 , Laura Elo 3, , Fu-Ping Zhang 1 , Suvi T Ruohonen 1 , Leena Strauss 1 , Michelangelo Foti 2 & Matti Poutanen 1
1Department of Physiology, Institute of Biomedicine and Turku Center for Disease Modeling University of Turku, Turku, Finland; 2Department of Cell Physiology and Metabolism, Faculty of Medicine, Centre Médical Universiatire, Geneva, Switzerland; 3Turku Centre for Biotechnology, University of Turku and Æbo Akademi University, Turku, Finland; 4Institute of Pathology, Technische Universität München, Munich, Germany; 5Department of Mathematics and Statistics, University of Turku, Turku, Finland.
: Hydroxysteroid (17beta) dehydrogenases (HSD17Bs) form a group of enzymes that are characterized by their sequence similarity at the active site, and their ability to catalyze the conversion between the weak 17keto- and the highly active 17beta-hydroxysteroids. To study the physiological role of HSD17B13, a lipid droplet associated protein, we characterized the phenotype of knockout (KO) mice deficient in HSD17B13 (HSD17B13KO). The data revealed normal serum sex steroid concentrations and proper reproductive performance in both male and female HSD17B13KO mice, indicating a minor role for HSD17B13 in sex steroid metabolism and reproduction. In line with the strong expression in the liver, histological analysis showed the presence of liver steatosis in HSD17B13KO mice that was associated with inflammation. The phenotype was more pronounced in males than females. The severity of the phenotype progressed with aging, and accumulation of triglycerides was observed in the livers of the male mice from 3 months onwards. Furthermore, metabolic profiling showed a tendency for increased hepatic phospholipid content in the 9 month-old HSD17B13KO males with two acylcarnitines (C16:0 and C18:1) showing the most profound increase (~2-fold). Additionally, presence of microgranulomas (Kupffer cell aggregations) with increased portal inflammation and ductular proliferation was observed in liver specimens from HSD17B13KO mice. This was associated with increased expression of immune response genes in the HSD17B13KO male liver. In conclusion, the lack of HSD17B13 impairs hepatic lipid metabolism in mice, resulting in liver steatosis and inflammation. The data, thus, indicate that HSD17B13 is involved in fatty acid metabolism in the liver, while the enzyme does not play a major role in the regulation of reproductive functions.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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