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Linder, K. ; Schleger, F. ; Kiefer-Schmidt, I.* ; Fritsche, L. ; Kümmel, S.* ; Heni, M. ; Weiss, M.* ; Häring, H.-U. ; Preissl, H. ; Fritsche, A.

Gestational diabetes impairs human fetal postprandial brain activity.

J. Clin. Endocrinol. Metab. 100, 4029-4036 (2015)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 0021-972X
e-ISSN 1945-7197
Quellenangaben Band: 100, Heft: 11, Seiten: 4029-4036 Artikelnummer: , Supplement: ,
Verlag Endocrine Society
Verlagsort Bethesda, Md.
Begutachtungsstatus Peer reviewed