ALPL 缺陷加速高脂诱导小鼠肝内脂肪沉积.

Objective: To clarify the role of the liver/bone/kidney alkaline phosphatase gene (ALPL) in high-fat diet-induced hepatic fat deposition. Methods: A fatty liver model was induced by administration of high-fat diet in wild-type (WT) and ALPL knockout (ALPL+/-) mice for 8 weeks. Intrahepatic fat deposition and serum glucose, triglyceride and cholesterol levels in serum were measured. RT-PCR, Western blotting and immunofluorescence staining were used to detect the expression of genes related to fatty acid synthesis and transport in liver. Results: No significant change in liver of fat deposition was observed in the ALPL+/- group compared with the WT group on normal diet, while serum glucose and cholesterol levels were increased; under high-fat conditions, intrahepatic fat deposition in the ALPL+/- mice was significantly increased and accompanied by an increase in serum triglyceride. RT-PCR and Western blotting results showed that the expression of the key fatty acid synthesis genes ACC1, ACC2 and PPAR-γ, and the fatty acid synthesis gene LPL in the liver of ALPL+/- mice were significantly increased under high-fat induction. In addition, immunofluorescence staining showed that PPAR-γ-positive hepatocytes were also significantly increased in the liver of ALPL+/- mice under high-fat induction. Conclusion: ALPL knockdown promotes the synthesis and transport of intrahepatic fatty acid and accelerates the fat deposition in the liver of mice induced by high fat. Our study provides potential theory to elucidate the molecular mechanism of liver steatosis. [ABSTRACT FROM AUTHOR]