ArticleJournal of anatomy2011
Glucose transporters GLUT4 and GLUT8 are upregulated after facial nerve axotomy in adult mice.
Article in Journal of anatomy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Motor neurons and endothelial cells additively promote development and fusion of human iPSC-derived skeletal myocytes.Skeletal muscle · 2024Article
- Review
- Aging alters glucose uptake in the naïve and injured rodent spinal cord.Neuroscience letters · 2019Article
- Glucose Transporters at the Blood-Brain Barrier: Function, Regulation and Gateways for Drug Delivery.Molecular neurobiology · 2017Review
- Expression and regulation of facilitative glucose transporters in equine insulin-sensitive tissue: from physiology to pathology.ISRN veterinary science · 2014Review
- The role of glucose transporters in brain disease: diabetes and Alzheimer’s Disease.International journal of molecular sciences · 2012Review
- Protective effect of insulin and glucose at different concentrations on penicillin-induced astrocyte death on the primer astroglial cell line.Neural regeneration research · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral nerve axotomy in adult mice elicits a complex response that includes increased glucose uptake in regenerating nerve cells. This work analyses the expression of the neuronal glucose transporters GLUT3, GLUT4 and GLUT8 in the facial nucleus of adult mice during the first days after facial nerve axotomy. Our results show that whereas GLUT3 levels do not vary, GLUT4 and GLUT8 immunoreactivity increases in the cell body of the injured motoneurons after the lesion. A sharp increase in GLUT4 immunoreactivity was detected 3 days after the nerve injury and levels remained high on Day 8, but to a lesser extent. GLUT8 also increased the levels but later than GLUT4, as they only rose on Day 8 post-lesion. These results indicate that glucose transport is activated in regenerating motoneurons and that GLUT4 plays a main role in this function. These results also suggest that metabolic defects involving impairment of glucose transporters may be principal components of the neurotoxic mechanisms leading to motoneuron death.
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Registered trials
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.