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青少年亚临床甲状腺功能减退对糖代谢的影响
作者:陈宇  张竞帆  刘聪  LI Ping  李玲 
单位:中国医科大学附属盛京医院 内分泌科, 辽宁 沈阳 110004
关键词:青少年 亚临床甲状腺功能减退 葡萄糖代谢 胰岛素抵抗 胰岛细胞功能 
分类号:R581.2
出版年·卷·期(页码):2020·39·第一期(8-13)
摘要:

目的:探讨亚临床甲状腺功能减退(SCH)对胰岛素抵抗和胰岛B细胞功能的影响。方法:共有92名中学生志愿者行75 g口服葡萄糖刺激胰岛素释放试验(OGIRT),同时测定甲状腺功能。采用HOMA-IR、松田指数(MI)等指标评价胰岛素抵抗。胰岛B细胞功能的评估包括HOMA-β,血胰岛素/葡萄糖之值,以及多种由OGIRT计算出的参数。结果:SCH组较甲状腺功能正常(ET)组OGIRT后120 min血糖显著升高[(7.39±1.07) mmol·L-1 vs (6.53±1.24) mmol·L-1P=0.021],糖耐量异常的发生率显著升高(53.85 vs 18.99,P=0.017)。SCH组的MI显著降低(33.33±10.32 vs 59.59±27.18,P=0.001),HOMA-IR显著升高[7.61(5.62~9.66) vs 4.04(2.96~5.87),P=0.002]。SCH组较ET组HOMA-β显著升高[318.52(285.87~387.69) vs 217.69(143.79~302.01),P=0.001],两组间糖负荷后胰岛素曲线下面积较空腹的增量(ΔAUCins),以及其与血糖曲线下面积增量的比值(ΔAUCins/ΔAUCglu)差异无统计学意义,反映胰岛素早相分泌的ΔAUCins30/ΔAUCglu30差异也无统计学意义。结论:SCH较ET者血糖升高,糖耐量异常发生率升高,存在着更为严重的胰岛素抵抗,空腹胰岛素分泌增加,而糖负荷后的胰岛素分泌没有差异。

Objective: To investigate the effects of subclinical hypothyroidism(SCH) on insulin resistance and islet B cell function. Methods: A total of 92 volunteer subjects were recruited in a secondary school setting for 75-g oral glucose-stimulated insulin release tests. HOMA-IR and Matsuda indexes were used to assess insulin resistance. The assessment of pancreatic islet B cell function comprised HOMA-β, blood insulin/glucose ratios, and indices derived from OGIRT. Results: The SCH group had significantly higher 120-minute post-OGIRT blood glucose levels [(7.39±1.07) mmol·L-1 vs (6.53±1.24) mmol·L-1, P=0.021] and prevalence of impaired glucose tolerance (IGT) (53.85 vs 18.99, P=0.017) compared to those in the euthyroid group(ET). The SCH group had significantly lower Matsuda index (33.33±10.32 vs 59.59±27.18, P=0.001), and higher HOMA-IR [7.61 (5.62-9.66) vs 4.04 (2.96-5.87), P=0.002] than those in the ET group. The SCH group had significantly elevated HOMA-β [318.52 (285.87-387.69) vs 217.69 (143.79-302.01), P=0.001]. There were no differences between the two groups withΔAUCins,ΔAUCins/ΔAUCglu and ΔAUCins30/ΔAUCglu30. Conclusion: The present study have provided evidence that subjects with SCH had higher blood glucose levels, increased prevalence and risk of IGT, more severe insulin resistance, and increased insulin secretion during fasting but not after glucose load compared to subjects with normal thyroid function.

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