Abnormal Glucose Metabolism and Insulin Sensitivity in Chinese Patients with Gitelman Syndrome
Abnormal Glucose Metabolism and Insulin Sensitivity in Chinese Patients with Gitelman Syndrome
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中国吉特曼综合征患者的血糖代谢异常和胰岛素敏感性
DOI：
10.1159/000346708
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发表时间：
2013-01-01
影响因子：
4.2
通讯作者：
Chen, Nan
中科院分区：
文献类型：
--
作者：
Ren, Hong;Qin, Ling;Chen, Nan
背景：Gitelman综合征（GS）是一种常染色体隐性肾小管病，主要特征为低钾性代谢性碱中毒，伴明显低镁血症、低尿钙、继发性醛固酮增多症和血压正常。据报道，低钾血症和低镁血症都会导致糖耐量受损和/或胰岛素抵抗，但尚不清楚糖耐量受损和/或胰岛素抵抗在 GS 患者中是否常见。方法：对 16 名 GS 患者和 12 名健康成人作为对照对象进行口服葡萄糖耐量试验。测量空腹血糖和血清胰岛素水平，并在口服葡萄糖负荷后测量30、60、120和180分钟后的葡萄糖和血清胰岛素值。计算葡萄糖和胰岛素的曲线下面积（AUC）。结果：1 例患者存在单纯空腹血糖受损，2 例患者存在单纯糖耐量受损，1 例患者同时存在空腹血糖受损和糖耐量受损。六名患者被诊断患有2型糖尿病。与健康正常对照组相比，GS患者表现出较高的AUC葡萄糖水平[16.1（IQR 12.5-25.4 mEq.h/l）vs.13.0（IQR 11.9-13.7 mEq.h/l）； p < 0.05] 和 AUC 胰岛素水平 [81.0 (IQR 58.9-138 mu U. h/ml) vs. 46.4 (IQR 35.6-63.3 mu U. h/ml)； p < 0.01]。 GS 患者表现出胰岛素分泌峰值的延迟，这是在葡萄糖负荷后 120 分钟观察到的。 GS 患者胰岛素抵抗的稳态模型评估显着高于对照志愿者。 GS组胰岛素敏感性定量检查指数和胰岛素敏感性综合指数均显着低于对照组。结论：GS患者糖代谢和胰岛素分泌异常常见。推测低钾血症和低镁血症可能是主要原因。版权所有 (C) 2013 S. Karger AG，巴塞尔
Background: Gitelman syndrome (GS) is an autosomal recessive disease of renal tubulopathy, primarily characterized by hypokalemic metabolic alkalosis with significant hypomagnesemia, low urinary calcium, secondary aldosteronism and normal blood pressure. Both hypokalemia and hypomagnesemia were reported to cause impaired glucose tolerance and/or insulin resistance, but it is unclear whether impaired glucose tolerance and/or insulin resistance are common in GS patients. Methods: An oral glucose tolerance test was performed among 16 GS patients and 12 healthy adults as control subjects. Fasting glucose and serum insulin levels were measured and the values of glucose and serum insulin after 30, 60, 120 and 180 min were also measured after an oral glucose load. The area under curve (AUC) of glucose and insulin was calculated. Results: One patient had isolated impaired fasting glucose, 2 had isolated impaired glucose tolerance, and 1 had combined impaired fasting glucose and glucose tolerance. Six patients were diagnosed with type 2 diabetes mellitus. Compared with a healthy normal control group, GS patients showed a higher AUC glucose level [16.1 (IQR 12.5-25.4 mEq . h/l) vs. 13.0 (IQR 11.9-13.7 mEq . h/l); p < 0.05] and AUC insulin level [81.0 (IQR 58.9-138 mu U . h/ml) vs. 46.4 (IQR 35.6-63.3 mu U . h/ml); p < 0.01]. GS patients showed a delay of insulin secretion peak which was observed 120 min after a glucose load. Homeostasis model assessment of insulin resistance in GS patients was significantly higher than in control volunteers. Quantitative insulin sensitivity check index and insulin sensitivity index composite in the GS group were significantly lower than in the control group. Conclusion: Abnormal glucose metabolism and insulin secretion is common in GS patients. It is speculated that hypokalemia and hypomagnesemia may be the main cause. Copyright (C) 2013 S. Karger AG, Basel