Gestational diabetes mellitus, epigenetic age and offspring metabolism.
Gestational diabetes mellitus, epigenetic age and offspring metabolism.
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DOI：
10.1111/dme.14925
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发表时间：
2022-11
影响因子：
3.5
通讯作者：
Dabelea, Dana
中科院分区：
文献类型：
--
作者：
Kim, Catherine;Harrall, Kylie K.;Glueck, Deborah H.;Needham, Belinda L.;Dabelea, Dana
没有报告研究宫内暴露于妊娠期糖尿病(GDM)、子代表观遗传年龄加速(EAA)和子代胰岛素敏感性之间的关系。使用来自队列研究的数据，我们使用单独的回归模型对子女的实际年龄和性别进行了调整，检验了孕期糖尿病宫内暴露与大约10 岁的后代EAA之间的关系。我们还使用混合线性回归模型检验了EAA与更新的稳态模型评估胰岛素敏感性和分泌(HOMA2-S和HOMA2-β)之间的关系，这些测量是在大约10岁和16 年龄测量的，考虑了在调整子女的时间年龄和性别后重复测量的因素。与未暴露的子代(n=91)相比，暴露于妊娠期糖尿病的子代(n=988)具有更大的EAA或更大的外在年龄(β系数2.00，95%可信区间[0.71，3.28]，p=0.0025)，但不高于内在Eaa(β系数−0.07，95%CI[−0.71，0.57]，p=0.93)。外源性EAA与较低的胰岛素敏感性(β系数−0.018，95%CI[−0.035，−0.002]，p=0.03)和较高的胰岛素分泌(β系数0.018，95%CI[0.006，0.03]，p=0.003)相关，在进一步调整母婴肥胖测量后，这些关联持续存在。在母婴肥胖测量调整前后，没有观察到内源性EAA与胰岛素敏感性和分泌之间的关联。在这项研究中，暴露于GDM的儿童经历了更多的外源性EAA，这与较低的胰岛素敏感性和更高的胰岛素分泌有关。需要进一步的研究来确定这些联系的方向性。
No reports examine the relationship between in‐utero exposure to gestational diabetes mellitus (GDM), offspring epigenetic age acceleration (EAA), and offspring insulin sensitivity. Using data from a cohort study, we examined associations between GDM in‐utero exposure and offspring EAA at approximately 10 years of age, using separate regression models adjusting for offspring chronological age and sex. We also examined associations between EAA with updated homeostasis model assessment of insulin sensitivity and secretion (HOMA2‐S and HOMA2‐β) measured at approximately 10 and 16 years of age, using mixed linear regression models accounting for repeated measures after adjustment for offspring chronological age and sex. Compared to unexposed offspring (n = 91), offspring exposed to GDM (n = 88) had greater EAA or older extrinsic age compared to chronological age (β‐coefficient 2.00, 95% confidence interval [0.71, 3.28], p = 0.0025), but not greater intrinsic EAA (β‐coefficient −0.07, 95% CI [−0.71, 0.57], p = 0.93). Extrinsic EAA was associated with lower insulin sensitivity (β‐coefficient −0.018, 95% CI [−0.035, −0.002], p = 0.03) and greater insulin secretion (β‐coefficient 0.018, 95% CI [0.006, 0.03], p = 0.003), and these associations persisted after further adjustment for measures of maternal and child adiposity. No associations were observed between intrinsic EAA and insulin sensitivity and secretion, before or after adjustment for measures of maternal and child adiposity. In this study, children exposed to GDM experience greater extrinsic EAA, which is associated with lower insulin sensitivity and greater insulin secretion. Further studies are needed to determine the directionality of these associations.
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