Expression of hepatitis B virus proteins in transgenic mice alters lipid metabolism and induces oxidative stress in the liver.

Background/aims: Hepatitis B virus transgenic mice (HBV-Tg mice) have been widely used as animal models in the study of pathogenesis and control of hepatitis B. It is important for the evaluation of such animal models to define the physiological differences between HBV-Tg and wild-type mice. The aim of this research was to investigate whether the integrated system biology approach that combines proteomics and metabonomics describes the physiological changes and provides new insights into the pathogenesis of the early stages of HBV infection.

Methods: In this study the protein and metabolite profiles of the liver were established based on two-dimensional electrophoresis and HPLC/MS analysis.

Results: Several protein molecules, whose expression was altered in HBV-Tg mouse liver, were identified including protective enzymes against oxidative stress and regulatory proteins related to lipid metabolism. Metabonomics confirmed the potential derangement of lipid metabolism by discovering the intermediate and the final products of lipid metabolism that were markedly changed in transgenic mice.

Conclusions: This study demonstrated that HBV antigens could impair host cell lipid metabolism and induce modest oxidative stress in vivo.