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

R. Stienstra, Y. Haim, Y. Riahi, M.G. Netea, A. Rudich, G. Leibowitz

Research output: Contribution to journalArticleAcademicpeer-review

65 Citations (Scopus)

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 languageEnglish
Pages (from-to)1505-1516
JournalDiabetologia
Volume57
Issue number8
DOIs
Publication statusPublished - 2014

Keywords

  • endoplasmic-reticulum stress
  • unfolded protein response
  • pancreatic b-cell
  • insulin-secretion
  • proinflammatory response
  • protective role
  • kappa-b
  • pathway
  • metabolism
  • glucose

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