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- W2098035900 endingPage "114" @default.
- W2098035900 startingPage "83" @default.
- W2098035900 abstract "The incidence and severity of diabetic neuropathy are increased by poor glycemic control, indicating that excess glucose may be the biochemical trigger in the pathogenesis of diabetic neuropathy. The chapter explores that distal symmetrical polyneuropathy is the most commonly recognized form of diabetic neuropathy and is composed primarily of sensory deficits and symptoms, which generally predominate over motor involvement. The symptoms of sensory neuropathy vary depending on the class of nerve fiber involved. The loss of large sensory fibers diminishes light touch, proprioception, and mechanoreception. Loss of small fibers diminishes pain and temperature perception, predisposing to injuries that can lead to diabetic foot ulcers. The pathology of diabetic neuropathy is multifocal with changes in axons, Schwann cells, microvascular elements in the endoneurium, and extracellular matrix. Thus a critical feature of the etiology of neuropathies is the mechanisms by which raised extracellular glucose alters the pattern of gene expression, which constitutes cell phenotype." @default.
- W2098035900 created "2016-06-24" @default.
- W2098035900 creator A5057795207 @default.
- W2098035900 creator A5073994215 @default.
- W2098035900 date "2002-01-01" @default.
- W2098035900 modified "2023-09-27" @default.
- W2098035900 title "Are mitogen-activated protein kinases glucose transducers for diabetic neuropathies?" @default.
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