| First Author | Chen S | Year | 2018 |
| Journal | FASEB J | Volume | 32 |
| Issue | 9 | Pages | 4836-4847 |
| PubMed ID | 29579398 | Mgi Jnum | J:278942 |
| Mgi Id | MGI:6357067 | Doi | 10.1096/fj.201701508R |
| Citation | Chen S, et al. (2018) Response gene to complement 32 suppresses adipose tissue thermogenic genes through inhibiting beta3-adrenergic receptor/mTORC1 signaling. FASEB J 32(9):4836-4847 |
| abstractText | Our previous studies have shown that response gene to complement (RGC)-32 deficiency (Rgc32(-/-)) protects mice from diet-induced obesity and increases thermogenic gene expression in adipose tissues. However, the underlying mechanisms by which RGC-32 regulates thermogenic gene expression remain to be determined. In the present study, RGC-32 expression in white adipose tissue (WAT) was suppressed during cold exposure-induced WAT browning. Rgc32(-/-) significantly increased thermogenic gene expression in the differentiated stromal vascular fraction (SVF) of inguinal (i)WAT and interscapular brown adipose tissue (BAT). Rgc32(-/-) and cold exposure regulated a common set of genes in iWAT, as shown by RNA sequencing data. Pathway enrichment analyses showed that Rgc32(-/-) down-regulated PI3K/Akt signaling-related genes. Akt phosphorylation was also consistently decreased in Rgc32(-/-) iWAT, which led to an increase in beta3-adrenergic receptor (beta3-AR) expression and subsequent activation of mammalian target of rapamycin complex (mTORC)-1. beta3-AR antagonist SR 59230A and mTORC1 inhibitor rapamycin blocked Rgc32(-/-)-induced thermogenic gene expression in both iWAT and interscapular BAT. These results indicate that RGC-32 suppresses adipose tissue thermogenic gene expression through down-regulation of beta3-AR expression and mTORC1 activity via a PI3K/Akt-dependent mechanism.-Chen, S., Mei, X., Yin, A., Yin, H., Cui, X.-B., Chen, S.-Y. Response gene to complement 32 suppresses adipose tissue thermogenic genes through inhibiting beta3-adrenergic receptor/mTORC1 signaling. |
