Journal
SCIENCE SIGNALING
Volume 9, Issue 416, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.aac5472
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Funding
- Robert Wood Johnson Foundation
- AGA(American Gastroenterological Association)-Gilead Sciences Research Scholar Award in Liver Disease
- Pediatric Scientist Development Program [K12HD000850-29]
- Nutrition Obesity Research Center [P30DK056341]
- Washington University Digestive Disease Research Core Center [P30DK52574, HL-38180, DK-56260, R01-DK078187]
- American Heart Association [14PRE18320006]
- Washington University S. T. Olin Fellowship
- Washington University NIGMS (National Institute of General Medical Sciences) Institutional Training Grant in Cell and Molecular Biosciences [T32GM007067]
- NSF Graduate Student Fellowship [DGE-1143954]
- Washington University Biomedical Mass Spectrometry Research Facility [P41 GM103422, P30 DK020579]
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Trehalose is a naturally occurring disaccharide that has gained attention for its ability to induce cellular autophagy and mitigate diseases related to pathological protein aggregation. Despite decades of ubiquitous use as a nutraceutical, preservative, and humectant, its mechanism of action remains elusive. We showed that trehalose inhibited members of the SLC2A (also known as GLUT) family of glucose transporters. Trehalose-mediated inhibition of glucose transport induced AMPK (adenosine 5'-monophosphate-activated protein kinase)-dependent autophagy and regression of hepatic steatosis in vivo and a reduction in the accumulation of lipid droplets in primary murine hepatocyte cultures. Our data indicated that trehalose triggers beneficial cellular autophagy by inhibiting glucose transport.
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