ArticleScientific reports2016
SLC2A8 (GLUT8) is a mammalian trehalose transporter required for trehalose-induced autophagy.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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63 citing papers in PubMed, 111 citations in OpenAlex.
- Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
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- Targeting microglia-mediated neuroinflammation in Alzheimer's disease: mechanisms and therapeutic approaches.Frontiers in immunology · 2026Review
- Therapeutic Targeting of Viral Myocarditis with Natural Products and Herbal Medicines: From Immune-Inflammatory Mechanisms to Clinical Translation.Journal of inflammation research · 2026Review
- Intracellular lactate dynamics iniScience · 2025Article
- APOE4 impairs macrophage lipophagy and promotes demyelination of spiral ganglion neurons in mouse cochleae.Cell death discovery · 2025Article
- Autophagy in Tissue Repair and Regeneration.Cells · 2025Review
- The generation of stable microvessels in ischemia is mediated by endothelial cell derived TRAIL.Science advances · 2024Article
- Hepatic WDR23 proteostasis mediates insulin homeostasis by regulating insulin-degrading enzyme capacity.GeroScience · 2024Article
- Hepatocyte MMP14 mediates liver and inter-organ inflammatory responses to diet-induced liver injury.PNAS nexus · 2024Article
- Risks and Benefits of SGLT-2 Inhibitors for Type 1 Diabetes Patients Using Automated Insulin Delivery Systems-A Literature Review.International journal of molecular sciences · 2024Review
- Autophagy and hepatic lipid metabolism: mechanistic insight and therapeutic potential for MASLD.npj metabolic health and disease · 2024Review
- Trehalose-Bearing Carriers to Target Impaired Autophagy and Protein Aggregation Diseases.Journal of medicinal chemistry · 2023Review
- Profiling neuroprotective potential of trehalose in animal models of neurodegenerative diseases: a systematic review.Neural regeneration research · 2023Review
- The tetraspanin transmembrane protein CD53 mediates dyslipidemia and integrates inflammatory and metabolic signaling in hepatocytes.The Journal of biological chemistry · 2023Article
- Autophagy in peritoneal fibrosis.Frontiers in physiology · 2023Review
- Recent developments of neuroprotective agents for degenerative retinal disorders.Neural regeneration research · 2022Review
- SIRT1 selectively exerts the metabolic protective effects of hepatocyte nicotinamide phosphoribosyltransferase.Nature communications · 2022Article
- Pegylated arginine deiminase drives arginine turnover and systemic autophagy to dictate energy metabolism.Cell reports. Medicine · 2022Article
- Trehalose causes low-grade lysosomal stress to activate TFEB and the autophagy-lysosome biogenesis response.Autophagy · 2021Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
Trehalose is a disaccharide demonstrated to mitigate disease burden in multiple murine neurodegenerative models. We recently revealed that trehalose rapidly induces hepatic autophagy and abrogates hepatic steatosis by inhibiting hexose transport via the SLC2A family of facilitative transporters. Prior studies, however, postulate that intracellular trehalose is sufficient to induce cellular autophagy. The objective of the current study was to identify the means by which trehalose accesses the hepatocyte cytoplasm, and define the distal signaling mechanisms by which trehalose induces autophagy. We provide gas chromatographic/mass spectrometric, fluorescence microscopic and radiolabeled uptake evidence that trehalose traverses the plasma membrane via SLC2A8 (GLUT8), a homolog of the trehalose transporter-1 (Tret1). Moreover, GLUT8-deficient hepatocytes and GLUT8-deficient mice exposed to trehalose resisted trehalose-induced AMP-activated protein kinase (AMPK) phosphorylation and autophagic induction in vitro and in vivo. Although trehalose profoundly attenuated mTORC1 signaling, trehalose-induced mTORC1 suppression was insufficient to activate autophagy in the absence of AMPK or GLUT8. Strikingly, transient, heterologous Tret1 overexpression reconstituted autophagic flux and AMPK signaling defects in GLUT8-deficient hepatocyte cultures. Together, these data suggest that cytoplasmic trehalose access is carrier-mediated, and that GLUT8 is a mammalian trehalose transporter required for hepatocyte trehalose-induced autophagy and signal transduction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.