Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-3-6
pubmed:abstractText
Congenital malformations are the leading cause of perinatal death among infants of diabetic women. Abnormal fuel metabolism and hyperglycemia have been shown to disturb embryogenesis during the earliest pre- and postimplantation stages in mice. This review presents a new model to explain, in part, adverse pregnancy outcomes associated with diabetes. In this model, by altering gene expression in developing tissues, raised glucose concentrations led to premature programmed cell death in key progenitor cells of the mouse blastocyst or in emerging organ structures in the mouse postimplantation embryo, resulting in abnormal morphogenesis or miscarriage. Although recent studies are still somewhat speculative and have currently only been explored in the mouse, this paradigm is supported by examples in other cell systems, which include human-derived cell lines, thereby suggesting that these findings are also applicable to human pregnancy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1043-2760
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
78-82
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Hyperglycemia and apoptosis: mechanisms for congenital malformations and pregnancy loss in diabetic women.
pubmed:affiliation
Dept of Obstetrics and Gynecology, Washington University, St Louis, MO 63110, USA. moleyk@msnotes.wustl.edu
pubmed:publicationType
Journal Article, Review