National Institute for Health and Welfare, Helsinki, Finland.
PEDEGO Research Unit (Research Unit for Pediatrics, Dermatology, Clinical Genetics, Obstetrics and Gynecology), Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland.
J Clin Endocrinol Metab. 2019 Jul 1;104(7):2785-2795. doi: 10.1210/jc.2018-02743.
Maternal gestational diabetes mellitus (GDM) and prepregnancy overweight/obesity [body mass index (BMI) ≥25 kg/m2] might adversely affect offspring cardiometabolic health.
To assess the associations between maternal GDM and prepregnancy overweight/obesity with adult offspring cardiometabolic risk factors.
Longitudinal cohort study (ESTER Maternal Pregnancy Disorders Study and the Arvo Ylppö Longitudinal Study).
Province of Uusimaa and Northern Finland.
At a mean age of 24.1 ± 1.3 years, we classified offspring as offspring of mothers with GDM regardless of the prepregnancy BMI (OGDM; n = 193); normoglycemic mothers with prepregnancy overweight/obesity (ONO; n = 157); and normoglycemic mothers with prepregnancy BMI <25 kg/m2 (controls; n = 556).
We assessed the cardiometabolic biomarkers from blood and measured the blood pressure at rest and heart rate.
Compared with the controls, the OGDM and ONO groups had greater fasting glucose (1.6%; 95% CI, 0.1% to 3.1%; and 2.3%; 95% CI, 0.5% to 4.3%, respectively) and insulin (12.7%; 95% CI, 4.4% to 21.9%; and 8.7%; 95% CI, 0.2% to 17.8%). These differences attenuated to nonsignificance when adjusted for confounders and/or current offspring characteristics, including BMI or body fat percentage. The OGDM group had lower SHBG (men, -12.4%; 95% CI, -20.2% to -3.9%; women, -33.2%; 95% CI, -46.3% to -16.8%), high-density lipoprotein (-6.6%; 95% CI, -10.9% to -2.2%), and apolipoprotein A1 (-4.5%; 95% CI, -7.5% to -1.4%). These differences survived the adjustments. The heart rate and other biomarkers were similar among the groups.
Adult offspring of mothers with GDM have increased markers of insulin resistance and a more atherogenic lipid profile. These were only partly explained by confounders or current offspring adiposity. Maternal prepregnancy overweight/obesity was associated with impaired offspring glucose regulation, which was explained by confounders and/or current adiposity.
母体妊娠糖尿病（GDM）和孕前超重/肥胖（BMI≥25kg/m2）可能对后代的心脏代谢健康产生不利影响。
评估母体 GDM 和孕前超重/肥胖与成年后代心脏代谢危险因素之间的关联。
纵向队列研究（ESTER 母体妊娠障碍研究和 Arvo Ylppö 纵向研究）。
乌西玛省和北芬兰。
在平均年龄为 24.1±1.3 岁时，我们将后代分为患有 GDM 的母亲所生的后代（无论其孕前 BMI 如何，OGDM；n=193）、孕前超重/肥胖的正常血糖母亲（ONO；n=157）和孕前 BMI<25kg/m2 的正常血糖母亲（对照组；n=556）。
我们评估了来自血液的心脏代谢生物标志物，并测量了静息时的血压和心率。
与对照组相比，OGDM 和 ONO 组的空腹血糖水平更高（1.6%；95%置信区间，0.1%至 3.1%；2.3%；95%置信区间，0.5%至 4.3%）和胰岛素水平更高（12.7%；95%置信区间，4.4%至 21.9%；8.7%；95%置信区间，0.2%至 17.8%）。当调整混杂因素和/或当前后代特征（包括 BMI 或体脂百分比）后，这些差异不再具有统计学意义。OGDM 组的性激素结合球蛋白（SHBG）水平更低（男性，-12.4%；95%置信区间，-20.2%至-3.9%；女性，-33.2%；95%置信区间，-46.3%至-16.8%）、高密度脂蛋白（-6.6%；95%置信区间，-10.9%至-2.2%）和载脂蛋白 A1（-4.5%；95%置信区间，-7.5%至-1.4%）水平更低。这些差异在调整后仍然存在。各组之间的心率和其他生物标志物相似。
患有 GDM 的母亲的成年后代存在胰岛素抵抗标志物增加和更易患动脉粥样硬化的血脂谱。这些仅部分被混杂因素或当前后代肥胖所解释。孕前超重/肥胖与后代葡萄糖调节受损有关，这种情况可以通过混杂因素和/或当前肥胖来解释。
