Lipid deposition in liver cells: The influence of short form augmenter of liver regeneration.

BACKGROUND AND OBJECTIVE:The short form augmenter of liver regeneration (sfALR) is a novel human hepatotrophic growth factor. The aim of this study was to investigate the potential role of sfALR in NAFLD. METHODS:The free fatty acids (FFA) induced lipid accumulation in mouse liver parenchymal cells was examined by Oil Red O staining and triglyceride level determination. The cell cycle was determined by flow cytometry and the proliferation was assessed by CCK8. The expression levels of gfer, miR-122, srebp-1c, fas, dgat2, acc1 and Lrp1B were assessed by quantitative real-time PCR. Furthermore, the MAPK pathway was detected by western blot. RESULTS:The results showed that sfALR could alleviate the lipid accumulation in mice both in vivo and in vitro. sfALR relieved the proliferation inhibition and G2 arrest of mouse liver parenchymal cells induced by FFAs. Free fatty acids affected gfer expression in a time-and dose-dependent way. And sfALR suppressed JNK activation, increased miR-122 level and reduced fatty acid synthesis-related gene expression. CONCLUSION:These findings suggested that sfALR could alleviate the severity of fatty liver in mice.