Regulation of hepatic lipid metabolism in CB1-/- and Abcb4-/- -HBV surface protein transgenic mice

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Nonalcoholic fatty liver disease (NAFLD) is currently one of the most prevalent liver diseases ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) with fibrosis and cirrhosis. Other common liver diseases encompass HCV or HBV infections and cholestasis. The coexistence of HBV infection and NAFLD has become a common cause of liver damage due to the high prevalence of both entities. There are substantial studies citing the association of hepatic steatosis as a major risk factor for development of hepatocellular carcinoma (HCC) and mortality in chronic HBV infection. From the literature, it is known that the inhibition of CB1 receptor has hepatoprotective and anti-steatotic effects. Additionally, Abcb4 knockout mice showed an impairment of lipid homeostasis which is linked to liver injury and development of hepatic fibrosis. Keeping in view, the major role of hepatic lipid metabolism in the pathogenesis of chronic liver diseases, the present study was conducted to investigate the role of the endocannabinoid signaling system and Abcb4 knockout induced cholestasis in the hepatic lipid regulation in HBs transgenic mice.The overall objective of this dissertation was to study the hepatic lipid regulation in HBs transgenic mice on two different genetic background mutations (CB1-/- and Abcb4-/-) and its impact on disease development and progression.

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