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Marginal biotin deficiency is teratogenic.

J Zempleni1, D M Mock

  • 1Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, 72202, USA.

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
|January 13, 2000
PubMed
Summary

Marginal biotin deficiency during pregnancy is common and may cause metabolic issues. This condition, though not severe, is linked to fetal malformations, suggesting a teratogenic risk in humans.

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Area of Science:

  • Nutritional biochemistry
  • Developmental biology
  • Obstetrics

Background:

  • Substantial biotin deficiency occurs in many women during normal pregnancy.
  • This deficiency, while not causing overt symptoms, leads to metabolic derangements.
  • Evidence suggests marginal biotin deficiency is teratogenic, causing fetal malformations in mammals.

Purpose of the Study:

  • To investigate the teratogenic potential of marginal biotin deficiency during human pregnancy.
  • To explore the mechanisms underlying biotin transport and requirements during gestation.

Main Methods:

  • Analysis of data from a published multivitamin supplementation study.
  • Investigation of placental biotin transport mechanisms.
  • Assessment of biotin accumulation in proliferating versus quiescent cells.

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Main Results:

  • Indirect evidence suggests spontaneous marginal biotin deficiency in human gestation is teratogenic.
  • Biotin transport across the human placenta is inefficient.
  • Proliferating cells exhibit a five-fold higher biotin accumulation rate compared to quiescent cells.

Conclusions:

  • Marginal biotin deficiency during pregnancy poses a teratogenic risk.
  • Increased biotin demand during cell proliferation and histone biotinylation may contribute to deficiency.
  • Altered lipid and skeletal development metabolism due to reduced biotin-dependent enzyme activity are potential consequences.