Linder Katarzyna, Schleger Franziska, Kiefer-Schmidt Isabelle, Fritsche Louise, Kümmel Stefanie, Böcker Marlene, Heni Martin, Weiss Magdalene, Häring Hans-Ulrich, Preissl Hubert, Fritsche Andreas
Department of Internal Medicine (K.L., M.H., H.-U.H., A.F.), Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University Hospital Tübingen, Tübingen, Germany; fMEG Center, University of Tübingen (F.S., I.K.-S., S.K., M.W., H.P.), Tübingen, Germany; German Center for Diabetes Research, Neuherberg, Germany (K.L., F.S., L.F., M.H., H.-U.H., H.P., A.F.); Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen (K.L., F.S., L.F., M.H., H.-U.H., H.P., A.F.), Tübingen, Germany; Department of Obstetrics and Gynecology (I.K.-S.), University Hospital Tübingen, Tübingen, Germany; Department of Pharmacy and Biochemistry (H.P.), Faculty of Science, University of Tübingen, Tübingen, Germany.
J Clin Endocrinol Metab. 2015 Nov;100(11):4029-36. doi: 10.1210/jc.2015-2692. Epub 2015 Oct 14.
Gestational diabetes (GDM) influences the fetal phenotype.
In the present study, our aim was to determine the effect of GDM specifically on fetal brain activity.
Pregnant participants underwent an oral glucose tolerance test (OGTT, 75 g). At 0, 60, and 120 minutes, maternal metabolism was determined, and fetal auditory evoked fields were recorded with a fetal magnetoencephalographic device.
All measurements were performed at the fMEG Center in Tübingen.
Twelve women with GDM and 28 normal glucose-tolerant (NGT) pregnant women participated on a voluntary basis.
OGTT (75 g, 120 minutes) was used in this study.
Fetal auditory evoked response latencies were determined for this study.
In the fetuses of NGT women, latencies decreased between 0 and 60 minutes from 260 ± 90 to 206 ± 74 ms (P = .008) and remained stable until 120 minutes (206 ± 74 vs 230 ± 79, P =.129). In fetuses of women with GDM, there was no change in response latencies during OGTT (P = .11). Sixty minutes after glucose ingestion, fetal latencies in the GDM group were longer than in the NGT group (296 ± 82 vs 206 ± 74 ms, P = .001). Linear regression revealed a significant effect of maternal glucose, insulin levels, and insulin sensitivity on response latencies after 60 minutes.
Fetal postprandial brain responses were slower in the offspring of women with GDM. This might indicate that gestational diabetes directly affects fetal brain development and may lead to central nervous insulin resistance in the fetus.
妊娠期糖尿病（GDM）会影响胎儿表型。
在本研究中，我们的目的是确定GDM对胎儿脑活动的具体影响。
怀孕参与者接受口服葡萄糖耐量试验（OGTT，75克）。在0、60和120分钟时，测定母体代谢情况，并用胎儿脑磁图设备记录胎儿听觉诱发电场。
所有测量均在图宾根的胎儿脑磁图中心进行。
12名患有GDM的女性和28名糖耐量正常（NGT）的孕妇自愿参与。
本研究采用OGTT（75克，120分钟）。
本研究测定了胎儿听觉诱发电位潜伏期。
在糖耐量正常女性的胎儿中，潜伏期在0至60分钟之间从260±90毫秒降至206±74毫秒（P = 0.008），并在120分钟时保持稳定（206±74 vs 230±79，P = 0.129）。在患有GDM的女性胎儿中，OGTT期间反应潜伏期没有变化（P = 0.11）。摄入葡萄糖60分钟后，GDM组胎儿的潜伏期长于NGT组（296±82 vs 206±74毫秒，P = 0.001）。线性回归显示，母体葡萄糖、胰岛素水平和胰岛素敏感性对60分钟后的反应潜伏期有显著影响。
患有GDM的女性后代的胎儿餐后脑反应较慢。这可能表明妊娠期糖尿病直接影响胎儿脑发育，并可能导致胎儿中枢神经系统胰岛素抵抗。
