Pregnancy insulin, glucose, and BMI contribute to birth outcomes in nondiabetic mothers.

Pregnancy insulin, glucose, and BMI contribute to birth outcomes in nondiabetic mothers.
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怀孕胰岛素,葡萄糖和BMI为非糖尿病母亲的出生结果做出了贡献。

DOI:
10.2337/dc08-1111
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发表时间:
2008-11
期刊:
影响因子:
16.2
通讯作者:
Dunger DB
Dunger DB
中科院分区:
医学1区
文献类型:
--
作者:
Ong KK;Diderholm B;Salzano G;Wingate D;Hughes IA;MacDougall J;Acerini CL;Dunger DB

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我们调查了母体妊娠率的正常变化对出生大小和其他出生结果的影响。研究设计和方法--两组早产妇女,一组为回顾性研究(n = 3,158),一组为前瞻性研究(n = 668),在妊娠28周时进行口服葡萄糖激发试验。在回顾性研究中,婴儿出生率与常规出生记录有关。在前瞻性研究中,通过从出生到24个月大的皮褶厚度评估后代肥胖。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,(平均值± SEM)2.1 ± 0.8%(P = 0.006)辅助阴道分娩的绝对风险增加3.4 ± 0.8%(P < 0.0001)增加急诊剖宫产率,3.1 ± 0.7%(P < 0.0001)增加择期剖宫产率,46 ± 8 g(P < 0.0001)增加后代出生体重。在前瞻性研究中,巨大儿(出生体重>第90百分位数)与母亲的空腹血糖(比值比2.61/+1 mmol/l [95%CI 1.15-5.93])和孕前BMI(1.10/+1 kg/m2 [1.04-1.18])独立相关。母亲较高的空腹血糖(P = 0.004),较低的胰岛素敏感性(P = 0.01),和较低的胰岛素分泌(P = 0.02)是独立相关的更大的后代出生时肥胖。在产后随访期间,母亲体重与后代肥胖之间的相关性在3个月时消失,而孕前BMI与后代肥胖之间的相关性仅在12和24个月时明显(均P < 0.05)。结论:孕前BMI、孕期BMI、胰岛素敏感性和胰岛素分泌都与后代肥胖和巨大儿有关,可能是干预的独立目标,以优化出生结局和后代健康。
OBJECTIVE—We investigated the effects of normal variations in maternal glycemia on birth size and other birth outcomes. RESEARCH DESIGN AND METHODS—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. RESULTS—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/m2 [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). CONCLUSIONS—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.
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