Deterioration of insulin sensitivity and beta-cell function in overweight Hispanic children during pubertal transition: A longitudinal assessment
Deterioration of insulin sensitivity and beta-cell function in overweight Hispanic children during pubertal transition: A longitudinal assessment
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DOI：
10.1080/17477160600780423
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发表时间：
2006-01-01
影响因子：
--
通讯作者：
Cruz, Martha L.
中科院分区：
文献类型：
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作者：
Goran, Michael I.;Shaibi, Gabriel Q.;Cruz, Martha L.
目的.研究超重的西班牙裔2型糖尿病高危儿童1年胰岛素动力学变化与身体成分和青春期过渡的关系。实验设计。在132名西班牙裔儿童（70名男孩/62名女孩;年龄10.9 ± 1.8岁）中测定了胰岛素动力学、身体成分和成熟的纵向变化。方法.采用双能X线吸收法测定身体成分，体格检查确定坦纳分期。使用胰岛素改良的静脉内葡萄糖耐量试验测定胰岛素敏感性（SI）、对葡萄糖的急性胰岛素反应（AIR）和处置指数（DI; β细胞功能指数）。在基线和1年后进行这些测量。结果脂肪量增加了13%（3.0 kg），SI下降了24%。在重复测量方差分析中，即使在调整了基线脂肪量、年龄、性别和脂肪量变化后，1年内胰岛素敏感性的下降仍然非常显著。SI的下降不受坦纳分期的影响。然而，成熟早期的受试者显示出AIR的代偿性增加（即适当的β细胞代偿），而成熟后期的受试者则没有（即代偿不良）。结论.这些结果表明，未能增加空气响应SI下降可能是一个因素的发病机制的进展，儿童2型糖尿病在这个危险的人口。
Purpose. To examine 1-year changes in insulin dynamics in overweight Hispanic children at high-risk of type 2 diabetes as a function of body composition and pubertal transition. Experimental Design. Longitudinal changes in insulin dynamics, body composition and maturation were determined in 132 Hispanic children (70 boys/62 girls; aged 10.9 +/- 1.8 years). Methods. Body composition was determined by dual energy x-ray absorptiometry and Tanner stage by physical examination. Insulin sensitivity (SI), the acute insulin response to glucose (AIR) and the disposition index (DI; an index of beta-cell function) were determined using an insulin modified intravenous glucose tolerance test. These measures were conducted at baseline and 1-year later. Results. Fat mass increased by 13% (3.0 kg) and SI declined by 24%. In repeated measures analysis of variance, the fall in insulin sensitivity over 1 year remained highly significant even after adjusting for baseline fat mass, age, gender and change in fat mass. The fall in SI was not significantly influenced by Tanner stage. However, subjects in earlier maturation showed a compensatory increase in AIR (i.e. appropriate beta-cell compensation), whereas subjects in the latter stages of maturation did not (i.e. poor compensation). Conclusions. These results indicate that failure to increase AIR in response to the fall in SI may be one factor in the pathogenesis of the progression of pediatric type 2 diabetes in this at risk population.