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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-4-25
pubmed:abstractText
Maternal diabetes affects the development of the offspring by altering the uterine environment. We aimed to investigate the extent to which the blood flow (measured as Tissue Perfusion Units; TPU) to implantation sites and the expression of developmentally important genes in the offspring are affected by maternal diabetes. We measured mRNA levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), Bcl-2 associated X protein (Bax), B-cell lymphoma protein (Bcl-2), tumor suppressor protein-53 (p53), paired box protein-3 (Pax-3) and vascular endothelial growth factor-A (Vegf-A). Moreover, we studied the effect on uterine blood flow (TPU) and the expression of the genes exerted by embryonic maldevelopment (malformation or resorption). Streptozotocin induced diabetic (D) and non-diabetic (N) pregnant rats were used in the study. Blood flow (TPU) to implantation sites was measured by a laser Doppler flow meter, and gene expression was analyzed by RT-PCR. Maternal diabetes caused increased blood flow (TPU) to implantation sites compared with normal pregnancy. Furthermore, implantation sites of D rats containing malformed offspring showed impaired growth and decreased blood flow (TPU) compared with their littermates at all gestational days. Resorbed offspring from both N and D rats displayed increased blood flow (TPU) compared with their non-resorbed littermates. Moreover, we found that maternal diabetes causes decreased expression of genes involved in the oxidative stress defense system (CuZnSOD in non-malformed D11 embryos, MnSOD at all gestational time points, ECSOD and Gpx-1 at GD11-GD15, CAT and Gpx-2 at GD15), decreased expression of Pax-3 at GD11, and increased expression of Vegf-A at all gestational time points. We conclude that both maternal metabolism and embryonic developmental state affect the blood flow (TPU) to the implantation site. Maternal diabetes causes decreased expression of anti-oxidative enzymes and enhanced angiogenesis in the offspring in rats.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0143-4004
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
413-21
pubmed:meshHeading
pubmed-meshheading:18387670-Animals, pubmed-meshheading:18387670-Antioxidants, pubmed-meshheading:18387670-Diabetes, Gestational, pubmed-meshheading:18387670-Diabetes Mellitus, Experimental, pubmed-meshheading:18387670-Embryo, Mammalian, pubmed-meshheading:18387670-Embryo Implantation, pubmed-meshheading:18387670-Female, pubmed-meshheading:18387670-Fetus, pubmed-meshheading:18387670-Gene Expression, pubmed-meshheading:18387670-Male, pubmed-meshheading:18387670-Maternal-Fetal Relations, pubmed-meshheading:18387670-Models, Biological, pubmed-meshheading:18387670-Neovascularization, Pathologic, pubmed-meshheading:18387670-Placental Circulation, pubmed-meshheading:18387670-Pregnancy, pubmed-meshheading:18387670-Pregnancy Complications, Hematologic, pubmed-meshheading:18387670-Pregnancy Outcome, pubmed-meshheading:18387670-Rats, pubmed-meshheading:18387670-Rats, Sprague-Dawley, pubmed-meshheading:18387670-Regional Blood Flow, pubmed-meshheading:18387670-Streptozocin, pubmed-meshheading:18387670-Uterus
pubmed:year
2008
pubmed:articleTitle
Altered uterine perfusion is involved in fetal outcome of diabetic rats.
pubmed:affiliation
Department of Medical Cell Biology, Box 571, Husargatan 3, Uppsala University, SE-751 23 Uppsala, Sweden. sheller.zabihi@mcb.uu.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't