| First Author | Zhang C | Year | 2013 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 305 |
| Issue | 4 | Pages | E530-9 |
| PubMed ID | 23800883 | Mgi Jnum | J:203193 |
| Mgi Id | MGI:5525175 | Doi | 10.1152/ajpendo.00640.2012 |
| Citation | Zhang C, et al. (2013) Autophagy is involved in adipogenic differentiation by repressesing proteasome-dependent PPARgamma2 degradation. Am J Physiol Endocrinol Metab 305(4):E530-9 |
| abstractText | Animal studies have shown that autophagy is essential in the process of obesity. Here, we performed daily injection of the autophagy inhibitor chloroquine (CQ) in mice and found that systemic administration of CQ blocks high-fat diet-induced obesity. To investigate the potential underlying molecular mechanism, we employed genetic and pharmacological interventions in cultured preadipocytes to investigate the role of autophagy in the control of the expression of the adipogenic regulator peroxisome proliferatior-activated receptor-gamma (PPARgamma). We show that adipogenic differentiation of 3T3-L1 preadipocytes is associated with activation of autophagy and increased PPARgamma2 protein level. Treatment with CQ, shRNA-mediated knockdown, or genetic engineering-induced deletion of autophagy-related gene 5 (Atg5) promoted proteasome-dependent PPARgamma2 degradation and attenuated adipogenic differentiation. Therefore, activated autophagy increases PPARgamma2 stability and promotes adipogenic differentiation, and inhibition of autophagy may prevent high-fat diet-induced obesity and the consequential type 2 diabetes. |
