![]() Abundance of 24 proteins was significantly different ( p < 0.01) between WT and HT-LCHAD mice. Proteins with significant changes in abundance were identified by mass spectrometry. Proteomic analysis of liver tissues from WT-mice and HT-mice with no signs of HCC was conducted. None of the wild-type (WT) mice developed steatosis and HCC ( n = 39), whereas HT-LCHAD mice ( n = 41) showed steatosis and ~20% (8/41) developed liver masses with histological features of HCC. The LCHAD exon 15 deletion was embryonic lethal to the homozygous mice whereas heterozygous mice (HT) develop significant hepatic steatosis starting at young age (3 months old) and HCC at older age (>13 months old) without any evidence of fibrosis or cirrhosis. Here we report, for the first time, generation of a mouse model with a defect in long-chain 3-hydoxy acyl-CoA dehydrogenase (LCHAD). Little is known about NAFLD without cirrhosis as a risk for HCC. The incidence of both nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC) have been increasing at an alarming rate.
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