Autophagy: Roles in obesity-induced ER stress and adiponectin downregulation in adipocytes

Lijun Zhou, Feng Liu

Research output: Contribution to journalComment/debatepeer-review

51 Scopus citations


Accumulating 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.

Original languageEnglish (US)
Pages (from-to)1196-1197
Number of pages2
Issue number8
StatePublished - Nov 16 2010


  • Adipokine
  • Adiponectin
  • Autophagy
  • DsbA-L
  • ER stress
  • Obesity

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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