| First Author | Yin Y | Year | 2015 |
| Journal | Mol Cell Endocrinol | Volume | 417 |
| Pages | 20-6 | PubMed ID | 26363221 |
| Mgi Jnum | J:236147 | Mgi Id | MGI:5804768 |
| Doi | 10.1016/j.mce.2015.09.006 | Citation | Yin Y, et al. (2015) AMPK-dependent modulation of hepatic lipid metabolism by nesfatin-1. Mol Cell Endocrinol 417:20-6 |
| abstractText | The aim of this study was to characterize the mechanism by which peripheral nesfatin-1 regulates hepatic lipid metabolism. Continuous peripheral infusion of nesfatin-1 reduced adiposity and plasma levels of triglyceride and cholesterol. In mice fed high fat diet, peripheral nesfatin-1 significantly decreased hepatic steatosis measured by triglyceride content and oil red staining area and diameter. These alterations were associated with a significant reduction in lipogenesis-related transcriptional factors PPARgamma and SREBP1, as well as rate-limited enzyme genes such as acaca, fasn, gpam, dgat1 and dgat2. In primary hepatocytes, nesfatin-1 inhibited both basal and oleic acid stimulated triglyceride accumulation, which was accompanied by a decrement in lipogenesis-related genes and an increase in beta-oxidation-related genes. In cultured hepatocytes, nesfatin-1 increased levels of AMPK phosphorylation. Inhibition of AMPK by compound C blocked the reduction of triglyceride content elicited by nesfatin-1. Our studies demonstrate that nesfatin-1 attenuates lipid accumulation in hepatocytes by an AMPK-dependent mechanism. |
