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Reprod Toxicol. 2007 Jan;23(1):63-74. Epub 2006 Sep 1.

Maternal diabetes in vivo and high glucose concentration in vitro increases apoptosis in rat embryos.

Author information

1
Department of Medical Cell Biology, Uppsala University, Biomedical Center, PO Box 571, SE-751 23 Uppsala, Sweden. Mattias.Gareskog@medcellbiol.uu.se

Abstract

Apoptosis may be involved in diabetes-induced embryonic dysmorphogenesis. We estimated the occurrence of apoptosis in embryos of a rat model for diabetic pregnancy. We found decreased Bcl-2, increased Bax and cleaved Caspase 3 proteins in embryos from diabetic rats. Moreover, we found increased activation of Caspase 3 in cells from embryos previously exposed to a diabetes-like environment (in vivo, in vitro) compared to cells from control embryos, which was normalized by supplementation of N-acetylcysteine or apoptosis inhibitor. We detected increased propidium iodide uptake in embryonic cells exposed to maternal diabetes, a finding confirmed by vital staining. Additionally, we found increased dysmorphogenesis in embryos exposed to a diabetic environment in vivo and in vitro. Exposure to a diabetic milieu during organogenesis increases apoptosis in embryonic cells and dysmorphogenesis in embryos. Enhanced apoptotic rate may have a role in diabetic embryopathy by inducing disturbed embryonic maturation, increased rates of resorptions and congenital malformations.

PMID:
17034987
DOI:
10.1016/j.reprotox.2006.08.009
[Indexed for MEDLINE]

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