![]() Nonalcoholic steatohepatitis (NASH), a progressive metabolic liver disease, is one of the major consequences of the current obesity epidemic. In conclusion, these results suggest that leptin-mediated neovascularization coordinated with VEGF plays an important role in the development of liver fibrosis and hepatocarcinogenesis in NASH. Our in vitro study revealed that leptin exerted a proangiogenic activity in the presence of VEGF. The CD31-immunopositive neovessels were mainly localized either along the fibrotic septa or in the GST-P–positive lesions. Hepatic neovascularization and the expression of vascular endothelial growth factor (VEGF), a potent angiogenic factor, only increased in littermate rats, almost in parallel with fibrogenesis and carcinogenesis. In sharp contrast, liver fibrosis, glutathione- S-transferase placental form (GST-P)-positive preneoplastic lesions, and HCC developed in littermate rats but not in Zucker rats. Both Zucker and littermate rats showed marked steatohepatitis and elevation of oxidative stress markers ( e.g., thiobarbital acid reactive substances and 8-hydroxydeoxyguanosine). Zucker rats, which naturally develop leptin receptor mutations, and their lean littermate rats were fed a choline-deficient, amino acid–defined diet. ![]() The aim of this study was to elucidate the role of angiogenesis in the development of liver fibrosis and hepatocarcinogenesis in NASH. ![]() Angiogenesis has been shown to play an important role in the progression of chronic liver disease. Nonalcoholic steatohepatitis (NASH) may cause fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) however, the exact mechanism of disease progression is not fully understood.
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