Role of aquaglyceroporins and caveolins in energy and metabolic homeostasis.
BACKGROUND Non-alcoholic fatty liver disease (NAFLD) is one of the most frequent causes of liver diseases, with markedly increased prevalence. However, its mechanisms are not clear. The present study was undertaken to illustrate the role of caveolin-1 (cav1) and the scavenger receptor class B type 1 (SR-B1) in NAFLD. METHODS Adult male C57BL/6 mice were fed with a normal diet or high fat and cholesterol (HFC) diet for 14 weeks. The mice were sacrificed to collect plasma and harvest the liver; their plasma lipid concentration was measured. Hepatic cav1 and SR-B1 mRNA and protein expression were determined by real-time quantitative polymerase chain reaction (qPCR) and Western blotting, respectively. In order to study cav1 and SR-B1 distribution and change in hepatocytes, immunohistochemical analysis was performed. RESULTS HFC diet increased plasma lipids, induced NAFLD and increased the liver/body weight ratio. Compared to the control mice (n=6), the mRNA and protein levels of cav1 and SR-B1 in liver tissue of the NAFLD mice (n=12) increased significantly (cav1 mRNA: 1.536+/-0.226 vs 0.980+/-0.272, P<0.05; protein: 0.643+/-0.240 vs 0.100+/-0.130, P<0.01; SR-B1 mRNA: 1.377+/-0.125 vs 0.956+/-0.151, P<0.01; protein: 2.156+/-0.507 vs 0.211+/-0.211, P<0.01). Furthermore, both cav1 and SR-B1 immunoreactivity increased and their distribution was also changed, mainly in the plasma membrane of hepatocytes, cytoplasm and membrane of lipid droplets and around. CONCLUSION NAFLD is associated with increased concentration of plasma lipids and upregulation of hepatic cav1 and SR-B1 gene and protein expressions, which indicate that cav1 and SR-B1 might play crucial roles in the pathogenesis of NAFLD.