Fetal overnutrition and offspring insulin resistance and β-cell function: the Exploring Perinatal Outcomes among Children (EPOCH) study.
Fetal overnutrition and offspring insulin resistance and β-cell function: the Exploring Perinatal Outcomes among Children (EPOCH) study.
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DOI：
10.1111/dme.13417
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发表时间：
2017-10
期刊：
影响因子：
--
通讯作者：
Dabelea D
中科院分区：
文献类型：
--
作者：
Sauder KA;Hockett CW;Ringham BM;Glueck DH;Dabelea D
在一项针对不同种族后代的纵向观察研究中，探讨孕产妇子宫内暴露于糖尿病和肥胖症与后代胰岛素抵抗、β细胞功能和口腔倾向指数的关系。总共 445 名在子宫内暴露于 (n=81) 或未暴露于 (n=364) 母亲糖尿病的后代分别在平均 (sd) 年龄 10.5 (1.5) 和 16.5 (1.2) 岁时完成了两次空腹血液测量，并在第二次就诊时完成了口服葡萄糖耐量测试。我们使用线性混合模型和一般线性单变量模型来评估母亲糖尿病和孕前体重指数与后代结局的关联。母亲子宫内糖尿病预示着胰岛素抵抗会增加[更新的胰岛素抵抗稳态模型评估 (HOMA2-IR) 高出 18%，P=0.01；松田指数降低 19%，P=0.01，更新后的 β 细胞功能稳态模型评估 (HOMA2-β) 提高 9%，P=0.04]。孕前体重指数每增加 5 kg/m2，预示胰岛素抵抗就会增加（HOMA2-IR 增加 11%，P<0.001；松田指数降低 10%，P<0.001；HOMA2-β 增加 6%，P<0.001）。在两种暴露的组合模型中获得了类似的结果。调整后代BMI后，只有母亲糖尿病与较高的HOMA2-IR（β=1.12，P=0.03）和较低的松田指数（β=0.83，P=0.01）相关。这两种暴露均与早期胰岛素反应或口腔倾向指数无关。与未接触糖尿病或肥胖症相比，宫内暴露于糖尿病或肥胖症与后代胰岛素抵抗的相关性更大，这支持了胎儿营养过剩导致儿童期和青春期代谢异常的假设。
To examine the associations of intrauterine exposure to maternal diabetes and obesity with offspring insulin resistance, β-cell function and oral disposition index in a longitudinal observational study of ethnically diverse offspring. A total of 445 offspring who were exposed (n=81) or not exposed (n=364) to maternal diabetes in utero completed two fasting blood measurements at mean (sd) ages of 10.5 (1.5) and 16.5 (1.2) years, respectively, and an oral glucose tolerance test at the second visit. We used linear mixed models and general linear univariate models to evaluate the associations of maternal diabetes and pre-pregnancy BMI with offspring outcomes. Maternal diabetes in utero predicted increased insulin resistance [18% higher updated homeostatic model assessment of insulin resistance (HOMA2-IR), P=0.01; 19% lower Matsuda index, P=0.01 and 9% greater updated homeostatic model assessment of β-cell function (HOMA2-β), P=0.04]. Each 5-kg/m2 increase in pre-pregnancy BMI predicted increased insulin resistance (11% greater HOMA2-IR, P<0.001; 10% lower Matsuda index, P<0.001; 6% greater HOMA2-β, P<0.001). Similar results were obtained in a combined model with both exposures. After adjustment for offspring BMI, only maternal diabetes was associated with higher HOMA2-IR (β=1.12, P=0.03) and lower Matsuda index (β=0.83, P=0.01). Neither exposure was associated with early insulin response or oral disposition index. Intrauterine exposure to diabetes or obesity is associated with greater offspring insulin resistance than non-exposure, supporting the hypothesis that fetal overnutrition results in metabolic abnormalities during childhood and adolescence.
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影响因子：
16.2
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作者：
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通讯作者：
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