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|Title:||Autophagy is involved in adipogenic differentiation by repressesing proteasome-dependent PPARγ2 degradation|
Peroxisome proliferatior-activated receptor-γ2
Proteasome-dependent protein degradation
|Citation:||Zhang, C., He, Y., Okutsu, M., Ong, L.C., Jin, Y., Zheng, L., Chow, P., Yu, S., Zhang, M., Yan, Z. (2013-05-08). Autophagy is involved in adipogenic differentiation by repressesing proteasome-dependent PPARγ2 degradation. American Journal of Physiology - Endocrinology and Metabolism 305 (4) : E530-E539. ScholarBank@NUS Repository. https://doi.org/10.1152/ajpendo.00640.2012|
|Abstract:||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-γ (PPARγ). We show that adipogenic differentiation of 3T3-L1 preadipocytes is associated with activation of autophagy and increased PPARγ2 protein level. Treatment with CQ, shRNA-mediated knockdown, or genetic engineering-induced deletion of autophagy-related gene 5 (Atg5) promoted proteasome-dependent PPARγ2 degradation and attenuated adipogenic differentiation. Therefore, activated autophagy increases PPARγ2 stability and promotes adipogenic differentiation, and inhibition of autophagy may prevent high-fat dietinduced obesity and the consequential type 2 diabetes. © 2013 the American Physiological Society.|
|Source Title:||American Journal of Physiology - Endocrinology and Metabolism|
|Appears in Collections:||Staff Publications|
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