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 |
|---|---|
| Pages (from-to) | 1505-1516 |
| Number of pages | 12 |
| Journal | Diabetologia |
| Volume | 57 |
| Issue number | 8 |
| DOIs | |
| State | Published - 1 Jan 2014 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
-
SDG 3 Good Health and Well-being
Keywords
- Adipocyte
- Adipose tissue
- Apoptosis
- Autophagy
- Beta cell
- Diabetes
- ER stress
- Inflammation
- Insulin resistance
- Macrophage
- Obesity
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
Fingerprint
Dive into the research topics of 'Autophagy in adipose tissue and the beta cell: Implications for obesity and diabetes'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver