期刊
DIABETES
卷 51, 期 3, 页码 819-824出版社
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.51.3.819
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资金
- NINDS NIH HHS [NS22352] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS022352] Funding Source: NIH RePORTER
Chronic hyperglycemia results in a predominantly sensory neuropathy. Recent studies suggest that dorsal root ganglion (DRG) neurons comprise a specific target and may be responsible for the important complication of diabetic sensory neuropathy, since hyperglycemia for longer than 6 months results in a vactiolar ganglionopathy with associated radiculopathy and distal sensory neuropathy. We undertook morphometric analysis of L5 DRG neurons in seven diabetic rats and six age- and sex-matched littermates. Nerve conduction studies were also performed, and neuropathy was confirmed. Diabetes was induced with streptozotocin; duration of diabetes was 12 months. The DRG count for control rats was 15,304 +/- 991 neurons. Two of seven diabetic DRG counts were reduced, but the group mean count at 14,847 +/- 1,524 was not significantly reduced. The number of small neurons (type B) considerably exceeded that of large neurons (type A), at a ratio of 71:29. The percentage of large cells was significantly reduced in diabetic compared with control rats (P = 0.01). The large-diameter population can be subdivided into two groups; with this subdivision, the number of neurons <50 mum was not reduced in samples from diabetic rats, but the neurons of largest size ( greater than or equal to50 mum) were significantly reduced (by 41%).
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