Longitudinal study on pubertal insulin resistance
Longitudinal study on pubertal insulin resistance
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DOI：
10.2337/diabetes.50.11.2444
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发表时间：
2001-11-01
期刊：
影响因子：
7.7
通讯作者：
Gower, BA
中科院分区：
文献类型：
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作者：
Goran, MI;Gower, BA
此前的横断面研究表明，青春期与胰岛素敏感度降低有关(S)，但没有纵向研究详细检验这一变化。本研究是一项纵向研究，对60名儿童(男33名，女27名；高加索人32名，非裔美国人28名)在Tanner分期I期(年龄9.2±1.4岁)和随访2.0+/-0.6年后进行检查，其中29例仍处于Tanner分期I期，31例进展到Tanner分期III或IV期。用改良的甲苯丁胺静脉葡萄糖耐量试验和最小造模法测定S-I、急性胰岛素反应(AIR)和处置指数(DI)，用双能X线骨密度仪测定体脂质量，用计算机断层扫描测定内脏脂肪，并分析空腹血激素水平。在进展到Tanner III期的儿童中，S显著下降了32%(4.4+/-3.0至3.0+/-1.7×10(-4)min(-1)/[MU IU/ml])，空气增加了30%，DI下降了2 7%，空腹血糖(93.5+/-5.0至97.0+/-4.1 mg/dl)和胰岛素(14.3+/-8.1至18.6+/-11.0 MU/ml)显著升高。在仍处于Tanner I期的儿童中，S-I(6.4+/-3.1至7.4+/-3.5×10(-4)min(-1)/[muIU/ml])略有升高，但空气、空腹血糖和胰岛素无明显变化。在非裔美国人中，S-I的青春期下降更为一致；在控制了年龄、性别以及脂肪质量、内脏脂肪和脱脂质量的变化后，青春期下降仍然显著；在低、中、高体脂的儿童中也是如此。S的变化与空腹激素水平的变化无显著相关，而空气中的变化与雄烯二酮的变化显著相关(r=0.39；P=0.04)。青春期从坦纳I期过渡到坦纳III期与S-I减少32%、空腹血糖、胰岛素和空气增加相关。这些变化在性别、种族和肥胖方面都是相似的。DI的显著下降表明，β细胞功能保持不变，或者对S-I下降的β细胞反应不足。S-I的下降与体脂、内脏脂肪、胰岛素样生长因子-I、雄激素或雌二醇的变化无关。
Previous cross-sectional studies show that puberty is associated with a reduction in insulin sensitivity (S,), but no longitudinal studies have examined this change in detail. This study is a longitudinal study in 60 children (33 male and 27 female subjects; 32 Caucasian and 28 African-American) examined at Tanner stage I (age 9.2 +/- 1.4 years) and after 2.0 +/- 0.6 years of follow-up, by which time 29 children remained at Tanner stage I and 31 had progressed to Tanner stage III or IV. Tanner stage was assessed by physical examination. S-I, the acute insulin response (AIR), and the disposition index (DI) were determined by the tolbutamide-modified intravenous glucose tolerance test and minimal modeling, body fat mass was assessed by dual-energy X-ray absorptiometry, visceral fat was determined by computed tomography, and fasting blood was analyzed for hormone levels. In children progressing to Tanner stage III, S, fell significantly by 32% (4.4 +/- 3.0 to 3.0 +/- 1.7 x 10(-4)min(-1)/[mu IU/ml]), AIR increased by 30%, DI fell by 27%, and there was a significant increase in fasting glucose (93.5 +/- 5.0 to 97.0 +/- 4.1 mg/dl) and insulin (14.3 +/- 8.1 to 18.6 +/- 11.0 mu IU/ml). In children remaining at Tanner stage I, there was a slight increase in S-I (6.4 +/- 3.1 to 7.4 +/- 3.5 x 10(-4)min(-1)/[mu IU/ml]) with no significant change in AIR or fasting glucose and insulin. The pubertal fall in S-I was more consistent in African-Americans; remained significant after controlling for age, sex, and change in fat mass, visceral fat, and fat-free mass; and was similar in children at low, medium, and high body fat. Change in S, was not significantly related to change in fasting hormone levels, but change in AIR was significantly related to change in androstendione (r = 0.39; P = 0.04). Pubertal transition from Tanner stage I to Tanner stage III was associated with a 32% reduction in S-I, and increases in fasting glucose, insulin, and AIR. These changes were similar across sex, ethnicity, and obesity. The significant fall in DI suggests conservation in beta -cell function or an inadequate beta -cell response to the fall in S-I. The fall in S-I was not associated with changes in body fat, visceral fat, IGF-I, androgens, or estradiol.