Department of Internal Medicine and Clinical Nutrition, Sahlgrenska Academy, University of Gothenburg, Sweden; Dublin Institute of Technology, Trinity College Dublin, Ireland.
Department of Internal Medicine and Clinical Nutrition, Sahlgrenska Academy, University of Gothenburg, Sweden.
J Steroid Biochem Mol Biol. 2019 Feb;186:117-121. doi: 10.1016/j.jsbmb.2018.10.003. Epub 2018 Oct 8.
Vitamin D status is hypothesised to play a role in gestational glucose control. No studies to date have examined vitamin D in relation to changes in blood glucose in pregnancy. Thus, the aim was to examine if vitamin D in early pregnancy and vitamin D trajectory associate with blood glucose trajectory over pregnancy in a Swedish cohort. We also investigated the relation between maternal vitamin D status and excessive fetal growth.
In 2013-2014, pregnant women were recruited to the GraviD cohort study when registering at the antenatal clinics in south-west Sweden. In the present analysis, 1928 women were included. Women with preexisting diabetes and multifetal pregnancy were excluded. Random blood glucose was assessed according to routine practice, in first trimester (T1, gestational week 4-16), second trimester (T2, gestational week 17-27), early (T3a, gestational week 28-35) and late third trimester (T3b, gestational week 36-41). In T1 and T3a, serum 25-hydroxyvitamim D (25OHD) was analyzed by liquid chromatography tandem mass spectrometry. Large for gestational age (LGA), as a proxy of excessive fetal growth, was defined as body weight at birth above 2 standard deviations of the gender specific population mean. Adjusted linear regression, linear mixed models analysis and logistic regression analysis were used to study 25OHD in relation to T1 blood glucose, glucose trajectory and LGA, respectively.
Mean blood glucose increased during pregnancy (5.21 mmol/L in T1, 5.27 mmol/L in T2, 5.31 mmol/L in T3a and 5.34 mmol/L in T3b; p = 0.003). In T1, 25OHD was negatively associated with blood glucose, i.e. 25OHD ≥ 30 nmol/L was associated with 0.25-0.35 mmol/L lower glucose. T1 25OHD was also negatively associated with blood glucose trajectory. Higher T3 25OHD was associated with higher odds of LGA (p = 0.032).
Avoiding maternal vitamin D deficiency in early pregnancy is associated with lower blood glucose in early pregnancy and throughout pregnancy. Higher 25OHD in late pregnancy was associated with higher odds of LGA at birth.
维生素 D 状况被认为在妊娠期血糖控制中发挥作用。迄今为止，尚无研究探讨维生素 D 与妊娠期间血糖变化的关系。因此，本研究旨在探讨瑞典队列中妊娠早期维生素 D 及维生素 D 变化轨迹与妊娠期间血糖变化轨迹之间的关系。我们还研究了母体维生素 D 状况与胎儿过度生长之间的关系。
2013-2014 年，在瑞典西南部的产前门诊登记时，招募了 GraviD 队列研究的孕妇。在本分析中，纳入了 1928 名女性。排除了患有糖尿病前期和多胎妊娠的女性。根据常规检测，在妊娠早期（T1，妊娠 4-16 周）、妊娠中期（T2，妊娠 17-27 周）、妊娠晚期（T3a，妊娠 28-35 周）和妊娠晚期（T3b，妊娠 36-41 周）检测随机血糖。T1 和 T3a 时，通过液相色谱串联质谱法分析血清 25-羟维生素 D（25OHD）。将出生体重大于性别特定人群均值 2 个标准差定义为巨大儿（LGA），作为胎儿过度生长的替代指标。采用多元线性回归、线性混合模型分析和逻辑回归分析分别研究 25OHD 与 T1 血糖、血糖变化轨迹和 LGA 的关系。
妊娠期间血糖升高（T1 时为 5.21mmol/L，T2 时为 5.27mmol/L，T3a 时为 5.31mmol/L，T3b 时为 5.34mmol/L；p=0.003）。T1 时，25OHD 与血糖呈负相关，即 25OHD≥30nmol/L 与血糖降低 0.25-0.35mmol/L 相关。T1 时 25OHD 也与血糖变化轨迹呈负相关。T3 时 25OHD 升高与 LGA 的几率升高相关（p=0.032）。
妊娠早期避免母体维生素 D 缺乏与妊娠早期和整个妊娠期间的血糖降低有关。妊娠晚期 25OHD 升高与出生时 LGA 的几率升高相关。
