Ong Ken K, Diderholm Barbro, Salzano Giuseppina, Wingate Dianne, Hughes Ieuan A, MacDougall Jane, Acerini Carlo L, Dunger David B
MRC Epidemiology Unit, Institute of Metabolic Science, Cambridge, UK.
Diabetes Care. 2008 Nov;31(11):2193-7. doi: 10.2337/dc08-1111. Epub 2008 Aug 12.
We investigated the effects of normal variations in maternal glycemia on birth size and other birth outcomes.
Women in two unselected birth cohorts, one retrospective (n = 3,158) and one prospective (n = 668), underwent an oral glucose challenge at 28 weeks of gestation. In the retrospective study, glycemia was linked to routine birth records. In the prospective study, offspring adiposity was assessed by skinfold thickness from birth to age 24 months.
In the retrospective study, within the nondiabetic range (2.1-7.8 mmol/l), each 1 mmol/l rise in the mother's 60-min glucose level was associated with a (mean +/- SEM) 2.1 +/- 0.8% (P = 0.006) rise in absolute risk of assisted vaginal delivery, a 3.4 +/- 0.8% (P < 0.0001) rise in emergency cesarean delivery, a 3.1 +/- 0.7% (P < 0.0001) rise in elective cesarean delivery, and a 46 +/- 8 g (P < 0.0001) increase in offspring birth weight. In the prospective study, fetal macrosomia (birth weight >90th centile) was independently related to the mother's fasting glucose (odds ratio 2.61 per +1 mmol/l [95% CI 1.15-5.93]) and prepregnancy BMI (1.10 per +1 kg/m(2) [1.04-1.18]). The mother's higher fasting glycemia (P = 0.004), lower insulin sensitivity (P = 0.01), and lower insulin secretion (P = 0.02) were independently related to greater offspring adiposity at birth. During postnatal follow-up, the correlation between the mother's glycemia and offspring adiposity disappeared by 3 months, whereas prepregnancy BMI was associated with offspring adiposity that was only apparent at 12 and 24 months (both P < 0.05).
Prepregnancy BMI, pregnancy glycemia, insulin sensitivity, and insulin secretion all contribute to offspring adiposity and macrosomia and may be separate targets for intervention to optimize birth outcomes and later offspring health.
我们研究了孕妇血糖正常变化对出生体重及其他出生结局的影响。
在两个未经挑选的出生队列中，一个为回顾性队列（n = 3158），另一个为前瞻性队列（n = 668），孕妇在妊娠28周时接受口服葡萄糖耐量试验。在回顾性研究中，将血糖水平与常规出生记录相联系。在前瞻性研究中，从出生至24个月龄，通过皮褶厚度评估子代肥胖情况。
在回顾性研究中，在非糖尿病范围内（2.1 - 7.8 mmol/l），母亲60分钟血糖水平每升高1 mmol/l，辅助阴道分娩的绝对风险增加（均值±标准误）2.1±0.8%（P = 0.006），急诊剖宫产风险增加3.4±0.8%（P < 0.0001），择期剖宫产风险增加3.1±0.7%（P < 0.0001），子代出生体重增加46±8 g（P < 0.0001）。在前瞻性研究中，巨大儿（出生体重>第90百分位数）与母亲空腹血糖（每升高1 mmol/l比值比为2.61 [95%可信区间1.15 - 5.93]）及孕前BMI（每升高1 kg/m²为1.10 [1.04 - 1.18]）独立相关。母亲较高的空腹血糖水平（P = 0.004）、较低的胰岛素敏感性（P = 0.01）及较低的胰岛素分泌（P = 0.02）与子代出生时更高的肥胖程度独立相关。在产后随访期间，母亲血糖水平与子代肥胖程度之间的相关性在3个月时消失，而孕前BMI与子代肥胖程度的相关性仅在12个月和24个月时明显（均P < 0.05）。
孕前BMI、孕期血糖水平、胰岛素敏感性及胰岛素分泌均与子代肥胖及巨大儿有关，可能是优化出生结局及子代后期健康的不同干预靶点。
