GLUCOSE-METABOLISM ALTERATIONS IN FRIEDREICHS ATAXIA
GLUCOSE-METABOLISM ALTERATIONS IN FRIEDREICHS ATAXIA
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DOI：
10.1212/wnl.38.8.1292
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发表时间：
1988-08-01
期刊：
影响因子：
9.9
通讯作者：
DIDONATO, S
中科院分区：
文献类型：
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作者：
FINOCCHIARO, G;BAIO, G;DIDONATO, S
我们通过研究21例患者和对照组在口服葡萄糖耐量试验（OGTT）、IV葡萄糖负荷和IV精氨酸负荷前后的血糖、胰岛素、生长激素（GH）和胰高血糖素，来描述Friedreich共济失调（FA）相关的糖代谢异常。12例患者为葡萄糖正常耐受（NT），5例葡萄糖不耐受（IT），4例糖尿病（DM）。在OGTT期间，IT患者的胰岛素分泌增加并延迟。有趣的是，在精氨酸负荷期间，NT和IT以及DM患者的胰岛素释放显著降低。IT患者对OGTT的GH反应发生改变。精氨酸负荷后患者的血浆胰高血糖素显著高于对照组。结果表明FA与胰岛素抵抗相关，β-细胞缺乏和I型糖尿病这些改变可能与FA的原发性缺陷有遗传联系或代谢相关。它们的相互作用或独立作用是FA中糖代谢异常的原因。
We have characterized the abnormalities of glucose metabolism associated with Friedreich''s ataxia (FA) by studying plasma glucose, insulin, growth hormone (GH), and glucagon before and after an oral glucose tolerance test (OGTT), an IV glucose load, and an IV arginine load, in 21 patients and in controls. Twelve patients were normotolerant (NT) to glucose, five glucose-intolerant (IT), and four diabetic (DM). Insulin secretion of IT patients was increased and delayed during OGTT. Interestingly, the insulin release during arginine load was significantly decreased in NT and IT as well as in DM patients. The GH response to OGTT was altered in IT patients. Plasma glucagon after an arginine load was significantly higher in patients than in the controls. The results indicate that FA is associated with insulin resistance, .beta.-cell deficiency, and type I diabetes. These alterations might be genetically linked or metabolically related to the primary defect in FA. Their interplay or independent effects are responsible for abnormalities of glucose metabolism in FA.