| Literature DB >> 18094705 |
David R Tomlinson1, Natalie J Gardiner.
Abstract
Neurons have a constantly high glucose demand, and unlike muscle cells they cannot accommodate episodic glucose uptake under the influence of insulin. Neuronal glucose uptake depends on the extracellular concentration of glucose, and cellular damage can ensue after persistent episodes of hyperglycaemia--a phenomenon referred to as glucose neurotoxicity. This article reviews the pathophysiological manifestation of raised glucose in neurons and how this can explain the major components of diabetic neuropathy.Entities:
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Year: 2008 PMID: 18094705 DOI: 10.1038/nrn2294
Source DB: PubMed Journal: Nat Rev Neurosci ISSN: 1471-003X Impact factor: 34.870