Original Article

Accelerated embryonic development associated with increased risk of neural tube defects induced by maternal diet in offspring of SELH/Bc mice†

  1. Katharine L. Stoate,
  2. Muriel J. Harris,
  3. Diana M. Juriloff*

Article first published online: 17 SEP 2008

DOI: 10.1002/bdra.20497

Issue

Birth Defects Research Part A: Clinical and Molecular Teratology

Birth Defects Research Part A: Clinical and Molecular Teratology

Special Issue: Remembering Marcy Speer

Volume 82, Issue 10, pages 720–727, October 2008

Additional Information

How to Cite

Stoate, K. L., Harris, M. J. and Juriloff, D. M. (2008), Accelerated embryonic development associated with increased risk of neural tube defects induced by maternal diet in offspring of SELH/Bc mice. Birth Defects Research Part A: Clinical and Molecular Teratology, 82: 720–727. doi: 10.1002/bdra.20497

Author Information

  1. Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada

*Dept. of Medical Genetics, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC Canada V6T 1Z3

  1. †

    Presented at the Fifth International Neural Tube Defects Conference, Asilomar, California, Sept. 24–27, 2007.

Publication History

  1. Issue published online: 20 OCT 2008
  2. Article first published online: 17 SEP 2008
  3. Manuscript Accepted: 1 JUL 2008
  4. Manuscript Revised: 20 JUN 2008
  5. Manuscript Received: 28 APR 2008

Funded by

  • Canadian Institutes of Health. Grant Number: IGI-60760

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Keywords:

  • neural tube;
  • exencephaly;
  • diet;
  • neural folds;
  • embryology;
  • mouse;
  • genetic;
  • multifactorial

Abstract

BACKGROUND: The SELH/Bc mouse strain has a high risk of the NTD, exencephaly, caused by multifactorial genetics. All SELH/Bc embryos have delayed elevation of neural folds; some never elevate (future exencephalics). Maternal diets affect SELH/Bc exencephaly rates: 25–35% on Purina Diet 5015 versus 5–10% on Purina Diet 5001. We hypothesized that in SELH/Bc, the diets affect maternal blood glucose and embryonic developmental rate. METHODS: We compared mice fed the two diets. On GD 9.4 we tested maternal blood glucose and examined embryos for developmental age (somite count) and cranial neural fold morphology. We observed GD 14 exencephaly rates. RESULTS: Diet 5015 caused fivefold more exencephaly (40 vs. 7% on GD 14), significantly higher mean maternal blood glucose in replicate experiments (6.3 vs. 5.5, p < .05; 6.3 vs. 5.3 mmol/L, p < .05), and significantly higher mean litter somite count on GD 9.4 (18.4 vs. 15.0, p < .05; 16.7 vs. 14.4 somites, p < .05). Among midrange embryos (15–16 somites), embryos from Diet 5015 were significantly shifted to earlier stages of midbrain fold morphology and had significantly more distance between the tips of the folds (p < .05). CONCLUSIONS: In SELH/Bc mice, the 5015 diet causes higher maternal blood glucose, a faster overall embryonic developmental rate during neural tube closure, and delayed midbrain fold elevation relative to overall development. This pattern suggests that maternal dietary effects that modestly increase embryonic growth rate may exacerbate a lack of coordination between genetically delayed neural folds and normally developing underlying tissues, increasing risk of NTD. Birth Defects Research (Part A), 2008. © 2008 Wiley-Liss, Inc.

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