Postimplantation diabetic embryopathy
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Ulf J. Eriksson, Parri Wentzel
Using an inbred Sprague Dawley strain (L) with about 20% skeletal malformations when the mother is diabetic and inbred Wistar Furth rats (no diabetes-inducible skeletal malformations), a global gene linkage analysis of the skeletal malformations was performed with microsatellites, a study that yielded strong coupling of the malformations to 7 regions on chromosomes 4, 10, 14, 18, and 19 and a weaker coupling to 14 other loci in the genome; altogether we found loci on 16 chromosomes. Searching for candidate genes within a distance of 10 cM from each microsatellite yielded 18 genes that had been implicated in previous studies of diabetic embryopathy. These genes were involved in embryonic development/morphogenesis (Map1b, Shh, Tgfb3, Vegfa, Dvl2, Nf1, Gsk3b, Gap43, Tgfbr3, Gdf1, Csf1r),308–314 regulation of DNA/RNA metabolism (En2, Brcc3, Tp53),192,308,315–317 regulation of apoptosis (Nol3, Bak1),308 and cellular metabolism (Folr1, Akr1b1).149,168,315