| First Author | Kan J | Year | 2019 |
| Journal | J Cell Physiol | Volume | 234 |
| Issue | 11 | Pages | 21395-21406 |
| PubMed ID | 31069793 | Mgi Jnum | J:289245 |
| Mgi Id | MGI:6434712 | Doi | 10.1002/jcp.28748 |
| Citation | Kan J, et al. (2019) S100A16, a novel lipogenesis promoting factor in livers of mice and hepatocytes in vitro. J Cell Physiol 234(11):21395-21406 |
| abstractText | To investigate the role of S100 calcium-binding protein A16 (S100A16) in hepatic lipid metabolism, S100a16 transgenic, S100a16 knockdown, and wildtype C57BL/6 mice were fed either a high-fat diet (HFD) or normal-fat diet (NFD) for 16 weeks. The results showed that for HFD-fed mice, S100a16 transgenic mice showed significantly more severe fatty liver than other HFD-fed mice, with a significant increase in serum triglyceride (TG) concentration, with more and larger lipid droplets in the liver, whereas S100a16 knockdown mice were completely opposite, with liver fat lesions and TG serological changes being the mildest; for NFD-fed mice, liver fat accumulation and serum TG concentrations were significantly lower than those fed HFD, and no significant lipid droplets were found in the liver. Further, we found that calmodulin (CaM) interacts with S100A16, a member of the AMP-activated protein kinase (AMPK) pathway. Our research found that S100A16 regulates the AMPK pathway-associated protein by interacting with CaM to regulate liver lipid synthesis. S100A16 regulates liver lipid metabolism through the CaM/CAMKK2/AMPK pathway. Overexpression of S100A16 promotes the deterioration of fatty liver induced by HFD, and low expression of S100A16 can attenuate fatty liver. |
