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lüll Autophagy: roles in obesity-induced ER stress and adiponectin downregulation in adipocytes Zhou L; Liu FAutophagy 2010[Nov]; 6 (8): 1196-7Accumulating evidence strongly suggests that autophagy, which is induced by endoplasmic reticulum (ER) stress in adipocytes, may play an important role in obesity-induced insulin resistance and type 2 diabetes. Obesity induces ER stress in mouse adipose tissue, which correlates with reduced adiponectin levels. In 3T3-L1 adipocytes, induction of ER stress is sufficient to promote autophagy-dependent adiponectin degradation. In contrast, suppressing ER stress increases adiponectin levels in 3T3-L1 adipocytes and alleviates high fat diet-induced adiponectin downregulation in mice. The ER stress-induced adiponectin downregulation can also be suppressed by overexpression of DsbA-L, a newly identified protein involved in promoting adiponectin multimerization and stability. Taken together, our results show that ER stress-induced autophagy provides an important mechanism underlying obesity-induced adiponectin downregulation in adipocytes. In addition, increasing the expression levels of DsbA-L could be an effective approach to improve adiponectin biosynthesis and stability, thus improving insulin sensitivity: in cells and in vivo.|*Autophagy[MESH]|3T3-L1 Cells[MESH]|Adipocytes/*metabolism[MESH]|Adiponectin/*genetics/metabolism[MESH]|Animals[MESH]|Cell Survival[MESH]|Down-Regulation/*genetics[MESH]|Endoplasmic Reticulum/metabolism/*pathology[MESH]|Energy Metabolism[MESH]|Humans[MESH]|Mice[MESH]|Models, Biological[MESH]|Obesity/*genetics/*pathology[MESH]|Stress, Physiological[MESH] |