4.5 Editorial Material

Mystery solved: Trehalose kickstarts autophagy by blocking glucose transport

Journal

SCIENCE SIGNALING
Volume 9, Issue 416, Pages -

Publisher

AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.aaf1937

Keywords

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Funding

  1. Millennium Institute [P09-015-F]
  2. Fondo de Financiamiento de Centros de Investigacion en Areas Prioritarias (FONDAP) [15150012]
  3. Frick Foundation [20014-15]
  4. ALS Therapy Alliance [2014-F-059]
  5. Muscular Dystrophy Association [382453]
  6. Michael J. Fox Foundation for Parkinson's Research [9277]
  7. Fundacion Copec-Universidad Catolica [2013.R.40]
  8. Ecos-Conicyt [C13S02]
  9. Fondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT) [1140549]
  10. Office of Naval Research-Global (ONR-G) [N62909-16-1-2003]
  11. Amyotrophic Lateral Sclerosis Research Program Therapeutic Idea Award [AL150111]
  12. FONDECYT [3140388]
  13. Wellcome Trust [095317/Z/11/Z]
  14. National Institute for Health Research Bio-medical Research Unit in Dementia at Addenbrooke's Hospital
  15. Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) [CONICYT-USA2013-0003]

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Although vertebrates cannot synthesize the natural disaccharide trehalose, exogenous administration of trehalose to mammalian cells may be beneficial for protein misfolding disorders. In this issue, DeBosch et al. show that trehalose may also be useful in treating nonalcoholic fatty liver disease and identify inhibition of cellular glucose import through SLC2A (also known as GLUT) transporters as a mechanism by which trehalose stimulates autophagy through the adenosine monophosphate-activated protein kinase (AMPK).

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