title: Gestational hyperglycemia reprograms cardiac gene expression in rat offspring.
abstract: BackgroundRat fetuses with maternal pregestational hyperglycemia develop cardiac dysfunction, and their cardiac gene expression differs from that of healthy control fetuses near term. We hypothesized that cardiac gene expression and morphologic abnormalities of rat fetuses with maternal pregestational hyperglycemia become normal after birth.MethodsNine rats were preconceptually injected with streptozotocin to induce maternal hyperglycemia and nine rats served as controls. The hyperglycemia group comprised 82 mice and the control group 74 offspring fed by euglycemic dams. Hearts of the offspring were collected on postnatal days 0, 7, and 14, and processed for histologic and gene expression analyses.ResultsOn day 0, heart weight was increased, and expression of cardiac genes involved in contractility, growth, and metabolism was decreased in the hyperglycemia group. On day 7, although cardiomyocyte apoptosis was enhanced, most of the changes in gene expression had normalized in the hyperglycemia group. By day 14, the expression of genes important for myocardial growth, function, and metabolism was again abnormal in the hyperglycemia group.ConclusionMost cardiac gene expression abnormalities become transiently normal during the first week of life of offspring to hyperglycemic rats. However, by day 14, cardiac expressions of genes involved in growth, function, and metabolism are again abnormal in relation to control offspring.
authors.affiliation: Department of Obstetrics and Gynecology, University of Turku, Turku, Finland.
authors.forename: Lara
authors.initials: L
authors.lastname: Lehtoranta
authors.affiliation: Department of Obstetrics and Gynecology, University of Turku, Turku, Finland.
authors.forename: Anna
authors.initials: A
authors.lastname: Koskinen
authors.affiliation: Department of Obstetrics and Gynecology, University of Turku, Turku, Finland.
authors.forename: Olli
authors.initials: O
authors.lastname: Vuolteenaho
authors.affiliation: Department of Obstetrics and Gynecology, University of Turku, Turku, Finland.
authors.forename: Jukka
authors.initials: J
authors.lastname: Laine
authors.affiliation: Department of Obstetrics and Gynecology, University of Turku, Turku, Finland.
authors.forename: Ville
authors.initials: V
authors.lastname: Kytö
authors.affiliation: Department of Obstetrics and Gynecology, University of Turku, Turku, Finland.
authors.forename: Hanna
authors.initials: H
authors.lastname: Soukka
authors.affiliation: Department of Obstetrics and Gynecology, University of Turku, Turku, Finland.
authors.forename: Eeva
authors.initials: E
authors.lastname: Ekholm
authors.affiliation: Department of Obstetrics and Gynecology, University of Turku, Turku, Finland.
authors.forename: Juha
authors.initials: J
authors.lastname: Räsänen
mesh_terms: D000818:Animals; D001835:Body Weight; D016640:Diabetes, Gestational / Q000235:genetics; D005260:Female; D015870:Gene Expression; D006943:Hyperglycemia / Q000150:complications / Q000235:genetics*; D009206:Myocardium / Q000378:metabolism*; D009929:Organ Size; D011247:Pregnancy; D011248:Pregnancy Complications / Q000235:genetics*; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013311:Streptozocin / Q000008:administration & dosage
chemical_list: D013311:Streptozocin