The Role of Testosterone in Hepatocyte Apoptosis in High Fat Diet-Induced Non-Alcoholic Fatty Liver Disease

Overview

Objectives/Goals The objective of this study was to learn whether hepatocyte apoptosis exists in the rat high fat diet (HFD)-induced non-alcoholic fatty liver disease model, and if so, whether or not testosterone reverses these apoptotic effects. Methods/Materials Adult male rats were randomly placed into four groups: castrated rats on HFD, castrated rats with Testosterone replacement on HFD, intact rats on HFD, and intact rats on regular chow diet (RCD). The rats were fed ad libitum for 15 weeks, sacrificed, and liver tissue was collected for detection of apoptosis. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was performed to directly stain apoptotic cells brown. Western blot was used to evaluate concentrations of cleaved PARP (89 kDa), a common marker for cell apoptosis. Results Both the TUNEL assay and the Western blot showed that HFD notably increased hepatocyte apoptosis compared with RCD in intact rats. Furthermore, they also showed that testosterone replacement significantly reduced HFD-induced hepatocyte apoptosis in castrated rats. This provided evidence that testosterone did in fact reverse the apoptotic effects of NAFLD. Conclusions/Discussion It was ultimately concluded that testosterone treatment significantly reduces HFD-induced hepatocyte apoptosis in the rat liver. This study confirms the beneficial effect of testosterone on cell apoptosis associated with NAFLD, and may forge a path toward developing methods to eventually attenuate NAFLD in the future.

Awards (1)

• Second Place

Competition history

• CSEF 2011 Mammalian Biology · Entry S1207

Resources

• CSEF project summary ↗

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