Document Detail

Influence of maternal metabolism and parental genetics on fetal maldevelopment in diabetic rat pregnancy.
MedLine Citation:
PMID:  22374754     Owner:  NLM     Status:  MEDLINE    
The purpose of this study was to investigate the influence of parental transgenerational genetics and maternal metabolic state on fetal maldevelopment in diabetic rat pregnancy. Rats from an inbred malformation-resistant (W) strain, and an inbred malformation-prone (L) strain, were cross-mated to produce two different F(1) hybrids, WL and LW. Normal (N) and manifestly diabetic (MD) WL and LW females were mated with normal males of the same F(1) generation to obtain WLWL and LWLW F(2) hybrids. Maternal diabetes increased malformation and resorption rates in both F(2) generations. MD-WLWL offspring had higher resorption rate but similar malformation rate compared with the MD-LWLW offspring. Malformed MD-WLWL offspring presented with 100% agnathia/micrognathia, whereas malformed MD-LWL offspring had 60% agnathia/micrognathia and 40% cleft lip and palate. The MD-WL dams showed increased β-hydroxybutyrate levels and alterations in concentrations of several amino acids (taurine, asparagine, citrulline, cystine, glutamic acid, leucine, tyrosine, and tryptophan) compared with MD-LW dams. Fetal glyceraldehyde-3-phosphate dehydrogenase (Gapdh) activity and gene expression were more altered in MD-WLWL than MD-LWLW. Fetal gene expression of reactive oxygen species (ROS) scavenger enzymes was diminished in MD-WLWL compared with MD-LWLW. Glial cell line-derived neurotrophic factor and Ret proto-oncogene gene expression was decreased in both MD-WLWL and MD-LWLW fetuses, whereas increased bone morphogenetic protein 4 and decreased Sonic hedgehog homolog expression was found only in MD-LWLW fetuses. Despite identical autosomal genotypes, the WL and LW dams gave birth to offspring with markedly different malformation patterns. Together with fetal differences in enzymatic activity and expression of Gapdh, ROS scavengers, and developmental genes, these results may suggest a teratological mechanism in diabetic pregnancy influenced by maternal metabolism and parental strain epigenetics.
A Ejdesjö; P Wentzel; U J Eriksson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-02-28
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  302     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-16     Completed Date:  2012-07-17     Revised Date:  2012-08-30    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E1198-209     Citation Subset:  IM    
Dept. of Medical Cell Biology, Biomedical Centre, PO Box 571, SE-75123 Uppsala, Sweden.
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MeSH Terms
Aldehyde Reductase / genetics,  metabolism
Amino Acids / blood
Blood Glucose / metabolism
Diabetes Mellitus, Experimental / genetics*,  metabolism*
Dinoprost / analogs & derivatives,  blood
Epigenesis, Genetic / physiology
Gene Expression Regulation, Developmental / physiology
Gestational Age
Glyceraldehyde-3-Phosphate Dehydrogenases / genetics,  metabolism
Heart Defects, Congenital / genetics*,  metabolism*
Lipids / blood
Mandible / abnormalities
Pregnancy in Diabetics / genetics*,  metabolism*
Rats, Inbred WF
Rats, Sprague-Dawley
Reactive Oxygen Species / metabolism
Superoxide Dismutase / metabolism
Reg. No./Substance:
0/Amino Acids; 0/Blood Glucose; 0/Lipids; 0/Reactive Oxygen Species; 27415-26-5/8-epi-prostaglandin F2alpha; 551-11-1/Dinoprost; EC Reductase; EC 1.15.1.-/superoxide dismutase 1; EC Dismutase; EC dismutase 2; EC 1.2.1.-/Glyceraldehyde-3-Phosphate Dehydrogenases

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