Longitudinal association between IGFBP-1 levels and parameters of the metabolic syndrome in obese children before and after weight loss

Longitudinal association between IGFBP-1 levels and parameters of the metabolic syndrome in obese children before and after weight loss
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DOI:
10.3109/17477166.2010.544739
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发表时间:
2011-08-01
影响因子:
--
通讯作者:
Roth, Christian L.
Roth, Christian L.
中科院分区:
其他
文献类型:
--
作者:
Reinehr, Thomas;Kleber, Michaela;Roth, Christian L.

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背景资料。胰岛素样生长因子结合蛋白1(IGFBP-1)是胰岛素抵抗的标志物。我们假设IGFBP-1与代谢综合征(METS)有关,代谢综合征与胰岛素抵抗有关。方法:研究方法。我们检查了51名肥胖的高加索儿童(平均年龄12.1+/-2.3,其中55%为男性,平均体重指数[BMI]31.8+/-4.8 kg/m(2))。分别于干预开始时和干预结束时测定人体测量指标、青春期、肝脏超声、腰围、血压、空腹血清IGFBP-1、IGFBP-3、IGF-I、脂联素、瘦素、转氨酶、血糖、胰岛素、甘油三酯和高密度脂蛋白-胆固醇水平。结果。与IGF-I和IGFBP-3相比,IGFBP-1在横断面(腰围:r=-0.45,甘油三酯:r=-0.29;胰岛素:r=-0.31;HOMA:r=-0.30)和纵向分析(增量甘油三酯:r=-0.22;增量胰岛素:r=-0.25;HOMA:r=-0.62)。HOMA变化与IGFBP-1变化的相关性强于瘦素或脂联素的变化与HOMA变化的相关性。在根据体重指数、青春期阶段、年龄和性别调整的多元Logistic回归分析中,METS的风险与IGFBP1水平呈负相关(优势比:每增加一个IGFBP1单位:-0.05%可信区间:-0.08至-0.02;p=-0.019)。9例有MET的肥胖儿童IGFBP-1水平(1.6+/-1.3ngm/L)显著低于42例无METs的肥胖儿童(4.0ng/-3.8 ng/ml)。11例有脂肪肝的肥胖儿童血清IGFBP-1水平(1.5+/-1.3 ng/L)显著低于40例非脂肪肝肥胖儿童(4.2+/-4.1 ng/ml)。结论。IGFBP-1、胰岛素抵抗和蛋氨酸之间的密切关系表明,IGFBP-1可能是这些实体肥胖的一个有前途的标记物。这项研究注册在Clinicaltrials.gov(NCT00435734)上。
Background. Insulin-like growth factor binding protein 1 (IGFBP-1) is a marker of insulin resistance. We hypothesized that IGFBP-1 is associated with the metabolic syndrome (MetS), which is related to insulin resistance. Methods. We examined 51 obese Caucasian children (mean age 12.1 +/- 2.3, 55% male, mean body mass index [BMI] 31.8 +/- 4.8 kg/m(2)). Anthropometrical markers, pubertal stage, hepatic ultrasound, waist circumference, blood pressure, fasting serum IGFBP-1, IGFBP-3, IGF-I, adiponectin, leptin, transaminases, glucose, insulin, triglycerides, and HDL-cholesterol concentrations were determined at onset and the end of the one-year lifestyle intervention. Results. In contrast to IGF-I and IGFBP-3, IGFBP-1 correlated significantly to most parameters of the MetS in cross-sectional (waist circumference: r = -0.45, triglycerides: r = -0.29; insulin: r = -0.31; HOMA: r = -0.30) and longitudinal analyses (Delta triglycerides: r = -0.22;Delta Insulin: r = -0.25;. HOMA: r = -0.62). The association between changes of HOMA and changes of IGFBP-1 was stronger than the associations between changes of leptin or adiponectin, and changes of HOMA. The risk for the MetS was inversely related to IGFBP-1 levels (odds ratio: -0.05 per additional IGFBP-1 unit; 95% confidence interval: -0.08 up to -0.02; p = -0.019) in a multiple logistic regression analyses adjusted to BMI, pubertal stage, age, and gender. The nine obese children with the MetS had significantly lower IGFBP-1 levels (1.6 +/- 1.3 ngm/l) than the 42 obese children without the MetS (4.0 +/- 3.8 ng/ml). The eleven obese children with fatty liver assessed by ultrasound had significantly lower IGFBP-1 levels (1.5 +/- 1.3 ngm/l) than the 40 obese children without fatty liver (4.2 +/- 4.1 ng/ml). Conclusion. The strong relationships between IGFBP-1, insulin resistance, and the MetS suggest that IGFBP-1 might be a promising marker for these entities in obesity. This study is registered at clinicaltrials.gov (NCT00435734).