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Papers In Press, published online ahead of print August 29, 2006
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Dept. of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen 2100
Corresponding Author: larsbo{at}rh.dk
Maternal diabetes can cause fetal macrosomia and increased risk of obesity, diabetes and cardiovascular disease in adulthood of the offspring. Although increased transplacental lipid transport could be involved, the impact of maternal type 1-diabetes on molecular mechanisms for lipid transport in placenta is largely unknown. To examine whether maternal type 1-diabetes affects placental lipid metabolism, we measured lipids and mRNA expression of lipase encoding genes in placentas from women with type 1-diabetes (n=27) and a control group (n=21). The placental triglyceride concentration and mRNA expression of endothelial lipase (EL) and hormone sensitive lipase were increased in placentas from women with diabetes. The differences were more pronounced in women with diabetes and sub-optimal metabolic control than in women with diabetes and good metabolic control. Placental mRNA expression of lipoprotein lipase and lysosomal lipase were similar in women with diabetes and the control group. Immunohistochemistry showed EL protein in syncytiotrophoblasts facing the maternal blood and endothelial cells facing the fetal blood both in placentas from normal women and women with diabetes. The results suggest that maternal type 1-diabetes is associated with triglyceride accumulation and increased endothelial and hormone sensitive lipase gene expression in placenta and that optimal metabolic control reduces these effects.
Revised on August 21, 2006
Accepted on August 29, 2006
Placental triglyceride accumulation in maternal type 1-diabetes is associated with increased endothelial and hormone sensitive lipase gene expression
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