Abstract
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 language | English |
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Pages (from-to) | 1505-1516 |
Number of pages | 12 |
Journal | Diabetologia |
Volume | 57 |
Issue number | 8 |
DOIs | |
State | Published - Aug 2014 |
Externally published | Yes |
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).
Keywords
- Adipocyte
- Adipose tissue
- Apoptosis
- Autophagy
- Beta cell
- Diabetes
- ER stress
- Inflammation
- Insulin resistance
- Macrophage
- Obesity