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Gestational Diabetes Impairs Human Fetal Postprandial Brain Activity

Katarzyna Linder¹, Franziska Schleger¹, Isabelle Kiefer-Schmidt¹

¹Department 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.

The Journal of Clinical Endocrinology and Metabolism

|October 15, 2015

Context:

Gestational diabetes (GDM) influences the fetal phenotype.

Objective:

In the present study, our aim was to determine the effect of GDM specifically on fetal brain activity.

Design:

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.

Setting:

All measurements were performed at the fMEG Center in Tübingen.

Participants:

Twelve women with GDM and 28 normal glucose-tolerant (NGT) pregnant women participated on a voluntary basis.

Interventions:

OGTT (75 g, 120 minutes) was used in this study.

Main Outcomes And Measures:

Fetal auditory evoked response latencies were determined for this study.

Results:

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.

Conclusions:

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.

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