| First Author | Zhao J | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 491 |
| Issue | 2 | Pages | 508-514 |
| PubMed ID | 28668388 | Mgi Jnum | J:251424 |
| Mgi Id | MGI:6103599 | Doi | 10.1016/j.bbrc.2017.06.149 |
| Citation | Zhao J, et al. (2017) AMPKalpha1 deficiency suppresses brown adipogenesis in favor of fibrogenesis during brown adipose tissue development. Biochem Biophys Res Commun 491(2):508-514 |
| abstractText | Brown adipose tissue (BAT) dissipates energy for thermogenesis which reduces or prevents obesity and metabolic dysfunction. AMP-activated protein kinase (AMPK) is a master regulator of energy metabolism and its activity is inhibited in the developing BAT due to obesity. We previously found that AMPK is required for brown fat development and thermogenic function, but the non-brown adipogenic differentiation of progenitor cells due to AMPKalpha1 deficiency has not been defined. We found that, in vivo, the thermogenic capacity and morphology of BAT were compromised due to AMPK deficiency, which was correlated with decreased progenitor density in BAT. In addition, the expression of fibrogenic markers was higher in AMPK deficient compared to wild-type mice. Furthermore, we transplanted AMPKalpha1 wild-type (WT) and floxed BAT into the same recipient mice; following tamoxifen induced AMPKalpha1 knockout in floxed BAT, the fibrogenesis was enhanced compared to WT mice. Taken together, our data demonstrated that AMPKalpha1 deficiency suppressed brown adipogenesis in favor of fibrogenesis during BAT development. |
