| First Author | Liu P | Year | 2018 |
| Journal | Cell Death Dis | Volume | 9 |
| Issue | 5 | Pages | 525 |
| PubMed ID | 29743578 | Mgi Jnum | J:262525 |
| Mgi Id | MGI:6163947 | Doi | 10.1038/s41419-018-0596-8 |
| Citation | Liu P, et al. (2018) Grail is involved in adipocyte differentiation and diet-induced obesity. Cell Death Dis 9(5):525 |
| abstractText | Grail is a crucial regulator of various biological processes, including the development of T-cell anergy, antiviral innate immune response, and cancer. However, the role of Grail in adipogenesis and obesity remains unclear. Here, we demonstrated that Grail knockdown in vitro leads to a decrease in PPARgamma expression, resulting in adipogenesis inhibition. However, Grail overexpression induced the same effects. Grail was shown to interact with PPARgamma, targeting it for degradation and modulating its adipogenic activity. PPARgamma expression was shown to be considerably reduced in Grail knockout (KO) mice fed normal diet or high-fat diet (HFD). The administration of both normal diet or HFD to Grail KO mice led to lower adipose mass and body weight than those in the wild-type mice. HFD-fed Grail KO mice had improved glucose and insulin tolerance. Taken together, our results indicate that Grail plays a pivotal role in adipogenesis and diet-induced obesity by regulating PPARgamma activity. |
