Autophagy in adipose tissue and the beta cell: Implications for obesity and diabetes

Rinke Stienstra, Yulia Haim, Yael Riahi, Mihai Netea, Assaf Rudich, Gil Leibowitz*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

86 Scopus citations


Autophagy is a lysosomal degradation pathway recycling intracellular long-lived proteins and damaged organelles, thereby maintaining cellular homeostasis. In addition to inflammatory processes, autophagy has been implicated in the regulation of adipose tissue and beta cell functions. In obesity and type 2 diabetes autophagic activity is modulated in a tissue-dependent manner. In this review we discuss the regulation of autophagy in adipose tissue and beta cells, exemplifying tissue-specific dysregulation of autophagy and its implications for the pathophysiology of obesity and type 2 diabetes. We will highlight common themes and outstanding gaps in our understanding, which need to be addressed before autophagy could be envisioned as a therapeutic target for the treatment of obesity and diabetes.

Original languageAmerican English
Pages (from-to)1505-1516
Number of pages12
Issue number8
StatePublished - Aug 2014
Externally publishedYes

Bibliographical note

Funding Information:
Funding This work was supported by grants from Deutsche Forschungsgemeinschaft (DFG): SFB 1052/1: ‘Obesity mechanisms’ (project B02, to AR) and by the Israel Science Foundation (347/12) to GL. RS is supported by a VIDI-grant from the Netherlands Organization for Scientific Research (NWO).


  • Adipocyte
  • Adipose tissue
  • Apoptosis
  • Autophagy
  • Beta cell
  • Diabetes
  • ER stress
  • Inflammation
  • Insulin resistance
  • Macrophage
  • Obesity


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