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母亲和胎儿 LEPR 常见变异与妊娠期间母体血糖特征的关联。

Association of maternal and fetal LEPR common variants with maternal glycemic traits during pregnancy.

机构信息

Department of Biology, Hainan Medical College, Haikou, Hainan, China.

Department of Gynaecology and Obstetrics, Taizhou People's Hospital, Taizhou, Jiangsu, China.

出版信息

Sci Rep. 2017 Jun 8;7(1):3112. doi: 10.1038/s41598-017-03518-x.

DOI:10.1038/s41598-017-03518-x
PMID:28596541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5465219/
Abstract

Recent studies suggested that maternal and placental leptin receptor (LEPR) may be involved in maternal glucose metabolism in pregnancy. To identify maternal and fetal LEPR common variants influencing gestational glycemic traits, we performed association study of 24-28-week maternal fasting glucose, glucose 1 hour after the consumption of a 50-g oral glucose load, fasting insulin and indices of beta-cell function (HOMA-β) and insulin resistance (HOMA-IR) in 1,112 unrelated women and their children. Follow-up of 36 LEPR loci identified 3 maternal loci (rs10889567, rs1137101 and rs3762274) associated with fasting glucose, these 3 fetal loci associated with fasting insulin and HOMA1-IR, as well as these 3 maternal-fetal loci combinations associated with HOMA2-β. We also demonstrated association of maternal locus rs7554485 with HOMA2-β and HOMA2-IR, maternal locus rs10749754 with fasting glucose, fetal locus rs10749754 with HOMA2-IR. However, these associations were no longer statistically significant after Bonferroni correction. In conclusion, our results first revealed multiple associations between maternal and fetal LEPR common variants and gestational glycemic traits. These associations did not survive Bonferroni correction. These corrections are overly conservative for association studies. We therefore believe the influence of these nominally significant variants on gestational glycometabolism will be confirmed by additional studies.

摘要

最近的研究表明,母体和胎盘瘦素受体(LEPR)可能参与妊娠期间的母体葡萄糖代谢。为了确定影响妊娠期血糖特征的母体和胎儿 LEPR 常见变异体,我们对 1112 名无关女性及其子女进行了 24-28 周的母体空腹血糖、口服 50 克葡萄糖负荷后 1 小时血糖、空腹胰岛素以及β细胞功能(HOMA-β)和胰岛素抵抗(HOMA-IR)的关联研究。对 36 个 LEPR 基因座的随访确定了 3 个与空腹血糖相关的母体基因座(rs10889567、rs1137101 和 rs3762274),这 3 个胎儿基因座与空腹胰岛素和 HOMA1-IR 相关,以及这 3 个母体-胎儿基因座组合与 HOMA2-β 相关。我们还证明了母体基因座 rs7554485 与 HOMA2-β 和 HOMA2-IR、母体基因座 rs10749754 与空腹血糖、胎儿基因座 rs10749754 与 HOMA2-IR 之间存在关联。然而,这些关联在经过 Bonferroni 校正后不再具有统计学意义。总之,我们的研究结果首次揭示了母体和胎儿 LEPR 常见变异体与妊娠期血糖特征之间的多种关联。这些关联在经过 Bonferroni 校正后不再具有统计学意义。这些校正对于关联研究来说过于保守。因此,我们认为这些名义上显著的变异体对妊娠期糖代谢的影响将通过额外的研究得到证实。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f33/5465219/44f09568250b/41598_2017_3518_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f33/5465219/44f09568250b/41598_2017_3518_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f33/5465219/44f09568250b/41598_2017_3518_Fig1_HTML.jpg

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