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[格雷夫斯病患者糖耐量异常的机制]

[The mechanism of glucose intolerance in patients with Graves' disease].

作者信息

Kondo Y, Suzuki S, Gomi Y, Mayumi K, Sakamaki T, Inoue T, Iino S

机构信息

Department of Internal Medicine, Showa University Fujigaoka Hospital.

出版信息

Nihon Naibunpi Gakkai Zasshi. 1992 Dec 20;68(12):1257-68. doi: 10.1507/endocrine1927.68.12_1257.

DOI:10.1507/endocrine1927.68.12_1257
PMID:1291337
Abstract

To investigate the mechanism of glucose intolerance in patients with Graves' disease, a 2-hour oral glucose tolerance test and euglycemic glucose clamp study using Biostator were performed in patients with Graves' disease and control subjects. 80 per cent of the patients showed impaired glucose tolerance. Insulinogenic index in the patients with borderline or diabetic glucose response was lower than that in subjects with normal glucose response. Insulinogenic index was inversely correlated with sigma PG during the test. Despite normal basal plasma glucose concentrations, basal plasma insulin levels in the patients with Graves' disease were higher than in the controls. Using the euglycemic glucose clamp technique, the glucose utilization rate (M value), the metabolic clearance rate of glucose (MCRG) and the insulin sensitivity index (M/I x 100) in the patients with Graves' disease were lower than in the controls. After treatment with antithyroid drug in 3 patients, glucose tolerance completely normalized, and there was a significant increase in the M value and the MCRG and a significant decrease in the metabolic clearance rate of insulin (MCRI) compared to the values before treatment. In the patients with Graves' disease, basal serum glucagon levels were higher than in the controls, and glucagon suppression during insulin infusion was found to be decreased. From these data, it is concluded that the decrease in glucose tolerance in patients with Graves' disease can be explained by 1) the impairment of early insulin release response to rapid intestinal glucose absorption, 2) increased insulin metabolic clearance and 3) hyperglucagonemia.

摘要

为研究格雷夫斯病患者糖耐量异常的机制,对格雷夫斯病患者和对照者进行了2小时口服葡萄糖耐量试验以及使用Biostator的正常血糖葡萄糖钳夹研究。80%的患者显示糖耐量受损。血糖反应处于临界值或糖尿病水平的患者的胰岛素生成指数低于血糖反应正常的受试者。试验期间胰岛素生成指数与餐后血糖标准差呈负相关。尽管基础血浆葡萄糖浓度正常,但格雷夫斯病患者的基础血浆胰岛素水平高于对照组。使用正常血糖葡萄糖钳夹技术,格雷夫斯病患者的葡萄糖利用率(M值)、葡萄糖代谢清除率(MCRG)和胰岛素敏感性指数(M/I×100)低于对照组。3例患者使用抗甲状腺药物治疗后,糖耐量完全恢复正常,与治疗前相比,M值和MCRG显著增加,胰岛素代谢清除率(MCRI)显著降低。在格雷夫斯病患者中,基础血清胰高血糖素水平高于对照组,且发现胰岛素输注期间胰高血糖素抑制作用降低。从这些数据得出结论,格雷夫斯病患者糖耐量降低可由以下原因解释:1)对快速肠道葡萄糖吸收的早期胰岛素释放反应受损;2)胰岛素代谢清除增加;3)高胰高血糖素血症。

相似文献

1
[The mechanism of glucose intolerance in patients with Graves' disease].[格雷夫斯病患者糖耐量异常的机制]
Nihon Naibunpi Gakkai Zasshi. 1992 Dec 20;68(12):1257-68. doi: 10.1507/endocrine1927.68.12_1257.
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Insulin sensitivity and exogenous insulin clearance in Graves' disease. Measurement by the glucose clamp technique and continuous indirect calorimetry.格雷夫斯病中的胰岛素敏感性和外源性胰岛素清除率。通过葡萄糖钳夹技术和连续间接测热法进行测量。
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Intern Med. 1995 May;34(5):339-41. doi: 10.2169/internalmedicine.34.339.
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beta-cell function and glucose and lipid oxidation in Graves' disease.格雷夫斯病中的β细胞功能以及葡萄糖和脂质氧化
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Glucose and insulin metabolism in patients with hyperthyroidism due to Graves' disease.格雷夫斯病所致甲状腺功能亢进症患者的葡萄糖和胰岛素代谢
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Insulin resistance in Graves' disease: a quantitative in-vivo evaluation.格雷夫斯病中的胰岛素抵抗:一项定量体内评估。
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Insulin secretion and sensitivity in hyperthyroidism.
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Methylprednisolone increases plasma leptin levels in Graves' hyperthyroidism patients with active Graves' ophthalmopathy.甲基强的松龙可提高伴有活动性格雷夫斯眼病的格雷夫斯甲状腺功能亢进症患者的血浆瘦素水平。
Horm Metab Res. 2000 Jul;32(7):277-82. doi: 10.1055/s-2007-978636.

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