| First Author | Huang Z | Year | 2024 |
| Journal | Sci Rep | Volume | 14 |
| Issue | 1 | Pages | 31464 |
| PubMed ID | 39732921 | Mgi Jnum | J:361378 |
| Mgi Id | MGI:7798423 | Doi | 10.1038/s41598-024-83112-0 |
| Citation | Huang Z, et al. (2024) Omentin-1 mitigates non-alcoholic fatty liver disease by preserving autophagy through AMPKalpha/mTOR signaling pathway. Sci Rep 14(1):31464 |
| abstractText | Adipose tissue-derived adipokines facilitate inter-organ communication between adipose tissue and other organs. Omentin-1, an adipokine, has been implicated in the regulation of glucose and insulin metabolism. However, limited knowledge exists regarding the regulatory impact of endogenous omentin-1 on hepatic steatosis. C57BL/6J mice were fed with high-fat diet (HFD) for 8 weeks to induce nonalcoholic fatty liver disease (NAFLD), while HepG2 cells were exposed to a 0.1 mM free fatty acid (FFA) mixture for 24 h to induce hepatic steatosis. Both the mice and cells were treated with omentin-1, and the therapeutic effects as well as the underlying molecular mechanisms were investigated. Our data demonstrate that omentin-1 attenuates weight and fat mass gain, preserves glucose homeostasis, normalizes the expression of lipogenesis-related proteins, and alleviates hepatic lipid accumulation in HFD fed mice. Furthermore, omentin-1 normalized AMPKalpha/mTOR signaling and preserves autophagy in these mice. In vitro, omentin-1 also preserves autophagy and attenuates lipid accumulation by normalizing AMPKalpha/mTOR signaling in a cell model of FFA treated HepG2 cells. However, inhibition of AMPK with Compound C or AMPKalpha whole-body knockout reverses the above beneficial effects of omentin-1. The present study demonstrates that omentin-1 exerts a preventive effect on non-alcoholic fatty liver disease (NAFLD) by preserving autophagy through normalizing the AMPKalpha/mTOR pathway, thereby suggesting its potential as a promising therapeutic agent against NAFLD. |
