Abstract
Background: During pregnancy, the placenta is an extremely important organ as it secretes its own hormones, e.g. insulin-like growth factor 1 (IGF-1), to ensure proper intrauterine fetal growth and development. Ethanol, an addictive and widely used drug, has numerous adverse effects during pregnancy, including fetal growth restriction (FGR). To date, the molecular mechanisms by which ethanol triggers its toxic effects during pregnancy, particularly in the placenta, are not entirely known. For this reason, a murine model of partial IGF-1 deficiency was used to determine ethanol alterations in placental morphology and AAH expression. Methods: Heterozygous (HZ, Igf1+/-) female mice were given 10% ethanol during 14 days as an acclimation period and throughout pregnancy. HZ female mice given water were used as controls. At gestational day 19, pregnant dams were sacrificed, placentas were collected and genotyped for subsequent studies. Results: IGF-1 deficiency and ethanol consumption during pregnancy altered placental morphology, and decreased placental efficiency and aspartyl/asparaginyl β-hydroxylase (AAH) expression in placentas from all genotypes. No differences were found in Igf1, Igf2, Igf1r and Igf2r mRNA expression in placentas from all groups. Conclusions: IGF-1 deficiency and ethanol consumption throughout gestation altered placental development, suggesting the crucial role of IGF-1 in the establishment of an adequate intrauterine environment that allows fetal growth. However, more studies are needed to study the precise mechanism to stablish the relation between both insults.
Highlights
Throughout pregnancy, the placenta is an essential organ for both mother and fetus; being the major determinant of intrauterine growth and serving as a protective barrier against external and internal insults.[1]Insulin-like growth factor 1 (IGF-1) is a pleiotropic hormone with several functions: mitochondrial protection,[2] cell proliferation and survival,[3] tissular growth and development.[4]
As either insulin-like growth factor 1 (IGF-1) deficiency or ethanol consumption during pregnancy produces fetal growth restriction (FGR), the aim of the present study was to determine whether IGF-1 partial deficiency is responsible for placental alterations in morphology and asparaginyl β-hydroxylase (AAH) expression, as well as if chronic ethanol exposure during gestation contributed to these placental changes
3.1 IGF-1 serum levels in pregnant dams chronically exposed to ethanol at gestational day 19 In order to validate IGF-1 serum levels in the present experimental model, control (WT) pregnant female mice treated with water or ethanol were used
Summary
Insulin-like growth factor 1 (IGF-1) is a pleiotropic hormone with several functions: mitochondrial protection,[2] cell proliferation and survival,[3] tissular growth and development.[4] It regulates placental morphogenesis and hormone secretion into umbilical and maternal circulations, processes that are indispensable for fetal development.[5] IGF-1, as well as insulin-like growth factor 2 (IGF-2), are key providers of placental resource allocation either for development or for response to external and environmental insults.[5,6,7] To this day, numerous IGF-1 deficiency conditions have been described in humans, e.g. fetal growth restriction (FGR).[8] FGR is a disorder where reduced levels in both IGF-1 and IGF-1 binding protein 3 (IGFBP-3) are observed, suggesting that reduced IGF-1 concentration in the fetus, mother and/or placenta may contribute to growth restriction.[8,9] FGR, among other harmful consequences, such as fetal death, miscarriage, low birth weight, premature birth and fetal alcohol spectrum disorders (FASD), can be a result of ethanol consumption during pregnancy .10,11. More studies are needed to study article can be found at the end of the article
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