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Mol Cell Endocrinol

Title:		A short periconceptional exposure to maternal type-1 diabetes is sufficient to disrupt the feto-placental phenotype in a rabbit model
Author(s):		Rousseau-Ralliard D; Couturier-Tarrade A; Thieme R; Brat R; Rolland A; Boileau P; Aubriere MC; Daniel N; Dahirel M; Derisoud E; Fournier N; Schindler M; Duranthon V; Fischer B; Santos AN; Chavatte-Palmer P;
Address:		"UMR BDR, INRA, ENVA, Universite Paris Saclay, 78350, Jouy en Josas, France. Electronic address: delphine.rousseau@inra.fr. UMR BDR, INRA, ENVA, Universite Paris Saclay, 78350, Jouy en Josas, France. Electronic address: anne.couturier-tarrade@inra.fr. Department of Anatomy and Cell Biology, Martin Luther University Faculty of Medicine, D-06097, Halle, Germany; Department of Visceral, Transplant, Thoracic and Vascular Surgery, University Hospital Leipzig, Leipzig, Germany. UMR BDR, INRA, ENVA, Universite Paris Saclay, 78350, Jouy en Josas, France. UVSQ (University of Versailles-Saint Quentin), Neonatal Medicine-CHIPS, 78303, Poissy, France. European Georges Pompidou Hospital, Biochemistry Unit, 75015, Paris, France. Department of Anatomy and Cell Biology, Martin Luther University Faculty of Medicine, D-06097, Halle, Germany"
Journal Title:		Mol Cell Endocrinol
Year:		2019
Volume:		20181009
Issue:
Page Number:		42 - 53
DOI:		10.1016/j.mce.2018.10.010
ISSN/ISBN:		1872-8057 (Electronic) 0303-7207 (Linking)
Abstract:		"Tight metabolic control of type-1 diabetes is essential during gestation, but it could be crucial during the periconception period. Feto-placental consequences of maternal type-1 diabetes around the time of conception need to be explored. Using a rabbit model, type-1 diabetes was induced by alloxan 7 days before mating. Glycemia was maintained at 15-20?ª+mmol/L with exogenous insulin injections to prevent ketoacidosis. At 4 days post-conception (dpc), embryos were collected from diabetic (D) or normoglycemic control (C) dams, respectively, and transferred into non-diabetic recipients. At 28dpc, D- and C-feto-placental units were collected for biometry, placental analyses and lipid profiles. D-fetuses were growth-retarded, hyperglycemic and dyslipidemic compared to C-fetuses. The efficiency of D-placentas was associated with an increased gene expression related to nutrient supply and lipid metabolism whereas volume density of fetal vessels decreased. Fetal plasma, placental and fetal liver membranes had specific fatty acid signatures depending on embryonic origin. Tissues from D-fetuses contained more omega-6 polyunsaturated fatty acids. The concentrations of docosahexaenoic acid decreased while linoleic acid increased in the heart of D-fetuses. This study demonstrates that a short exposure to maternal type-1 diabetes in the periconception window, until the blastocyst stage, is able to irreversibly malprogram the feto-placental phenotype, through precocious and persistent structural and molecular adaptations of placenta"
Keywords:		"Animals Diabetes Mellitus, Type 1/blood/genetics/*pathology Disease Models, Animal Dyslipidemias/complications/pathology Fatty Acids/blood Female Fetal Growth Retardation/blood/pathology Fetus/blood supply/*pathology Gene Expression Regulation, Developmen;"
Notes:		"MedlineRousseau-Ralliard, Delphine Couturier-Tarrade, Anne Thieme, Rene Brat, Roselyne Rolland, Audrey Boileau, Pascal Aubriere, Marie-Christine Daniel, Nathalie Dahirel, Michele Derisoud, Emilie Fournier, Natalie Schindler, Maria Duranthon, Veronique Fischer, Bernd Santos, Anne Navarrete Chavatte-Palmer, Pascale eng Research Support, Non-U.S. Gov't Ireland 2018/10/12 Mol Cell Endocrinol. 2019 Jan 15; 480:42-53. doi: 10.1016/j.mce.2018.10.010. Epub 2018 Oct 9"