Dataset Information

Relation of placental alkaline phosphatase expression in human term placenta with maternal and offspring fat mass.

ABSTRACT: INTRODUCTION:Alkaline phosphatase is implicated in intestinal lipid transport and in the development of obesity. Placental alkaline phosphatase is localised to the microvillous plasma membrane of the placental syncytiotrophoblast at the maternal-fetal interface, but its role is unclear. We investigated the relations of placental alkaline phosphatase activity and mRNA expression with maternal body composition and offspring fat mass in humans. METHODS:Term human placentas from the UK Birthright cohort (n?=?52) and the Southampton Women's Survey (SWS) (n?=?95) were studied. In the Birthright cohort, alkaline phosphatase activity was measured in placental microvillous plasma membrane vesicles. In the SWS, alkaline phosphatase mRNA was measured using Nanostring. Alkaline phosphatase gene expression was compared to other lipid-related genes. RESULTS:In Birthright samples placental microvillous plasma membrane alkaline phosphatase activity was positively associated with maternal triceps skinfold thickness and BMI (??=?0.04 (95% CI: 0.01-0.06) and ??=?0.02 (0.00-0.03) µmol/mg protein/min per SD, P?=?0.002 and P?=?0.05, respectively) after adjusting for potential confounders. In SWS samples placental alkaline phosphatase mRNA expression in term placenta was positively associated with maternal triceps skinfold (??=?0.24 (0.04, 0.44) SD/SD, P?=?0.02), had no association with neonatal %fat mass (??=?0.01 (-0.20 to 0.21) SD/SD, P?=?0.93) and was negatively correlated with %fat mass at ages 4 (??=?-0.28 (-0.52 to -0.04) SD/SD, P?=?0.02), 6-7 (??=?-0.25 (-0.49 to -0.02) SD/SD, P?=?0.03) years. When compared with placental expression of other genes, alkaline phosphatase expression was positively related to genes including the lysophosphatidylcholine transporter MFSD2A (major facilitator superfamily domain containing 2A, P?

SUBMITTER: Hirschmugl B

PROVIDER: S-EPMC6173293 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Relation of placental alkaline phosphatase expression in human term placenta with maternal and offspring fat mass.

Hirschmugl Birgit B Crozier Sarah S Matthews Nina N Kitzinger Eva E Klymiuk Ingeborg I Inskip Hazel M HM Harvey Nicholas C NC Cooper Cyrus C Sibley Colin P CP Glazier Jocelyn J Wadsack Christian C Godfrey Keith M KM Desoye Gernot G Lewis Rohan M RM

International journal of obesity (2005) 20180613 6

<h4>Introduction</h4>Alkaline phosphatase is implicated in intestinal lipid transport and in the development of obesity. Placental alkaline phosphatase is localised to the microvillous plasma membrane of the placental syncytiotrophoblast at the maternal-fetal interface, but its role is unclear. We investigated the relations of placental alkaline phosphatase activity and mRNA expression with maternal body composition and offspring fat mass in humans.<h4>Methods</h4>Term human placentas from the U ...[more]

PMID: 29899523

Similar Datasets

Project description:Over the last thirty years, evidence has been accumulating that Hypertensive Disorders of Pregnancy (HDP) and, specifically, Preeclampsia (PE) produce not only long-term effects on the pregnant woman, but have also lasting consequences for the fetus. At the core of these consequences is the phenomenon known as defective deep placentation, being present in virtually every major obstetrical syndrome. The profound placental vascular lesions characteristic of this pathology can induce long-term adverse consequences for the pregnant woman's entire arterial system. In addition, placental growth restriction and function can, in turn, cause a decreased blood supply to the fetus, with long-lasting effects. Women with a history of HDP have an increased risk of Cardiovascular Diseases (CVD) compared with women with normal pregnancies. Specifically, these subjects are at a future higher risk of: Hypertension; Coronary artery disease; Heart failure; Peripheral vascular disease; Cerebrovascular accidents (Stroke); CVD-related mortality. Vascular pathology in pregnancy and CVD may share a common etiology and may have common risk factors, which are unmasked by the "stress" of pregnancy. It is also possible that the future occurrence of a CVD may be the consequence of endothelial dysfunction generated by pregnancy-induced hypertension that persists after delivery. Although biochemical and biophysical markers of PE abound, information on markers for a comparative evaluation in the various groups is still lacking. Long-term consequences for the fetus are an integral part of the theory of a fetal origin of a number of adult diseases, known as the Barker hypothesis. Indeed, intrauterine malnutrition and fetal growth restriction represent significant risk factors for the development of chronic hypertension, diabetes, stroke and death from coronary artery disease in adults. Other factors will also influence the development later in life of hypertension, coronary and myocardial disease; they include parental genetic disposition, epigenetic modifications, endothelial dysfunction, concurrent intrauterine exposures, and the lifestyle of the affected individual.

Project description:Maternal overnutrition can affect fetal growth and development, thus increasing susceptibility to obesity and diabetes in later life of the offspring. Placenta is the central organ connecting the developing fetus with the maternal environment. It is indicated placental fatty acid metabolism plays an essential role in affecting the outcome of the pregnancy and fetus. However, the role of placental fatty acid β-oxidation (FAO) in maternal overnutrition affecting glucose metabolism in the offspring remains unclear. In this study, C57BL/6J female mice were fed with normal chow or high-fat diet before and during pregnancy and lactation. The placenta and fetal liver were collected at gestation day 18.5, and the offspring's liver was collected at weaning. FAO-related genes and AMP-activated protein kinase (AMPK) signaling pathway were examined both in the placenta and in the human JEG-3 trophoblast cells. FAO-related genes were further examined in the liver of the fetuses and in the offspring at weaning. We found that dams fed with high-fat diet showed higher fasting blood glucose, impaired glucose tolerance at gestation day 14.5 and higher serum total cholesterol (T-CHO) at gestation day 18.5. The placental weight and lipid deposition were significantly increased in maternal high-fat diet group. At weaning, the offspring mice of high-fat diet group exhibited higher body weight, impaired glucose tolerance, insulin resistance and increased serum T-CHO, compared with control group. We further found that maternal high-fat diet downregulated mRNA and protein expressions of carnitine palmitoyltransferase 2 (CPT2), a key enzyme in FAO, by suppressing the AMPK/Sirt1/PGC1α signaling pathway in the placenta. In JEG-3 cells, protein expressions of CPT2 and CPT1b were both downregulated by suppressing the AMPK/Sirt1/PGC1α signaling pathway under glucolipotoxic condition, but were later restored by the AMPK agonist 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR). However, there was no difference in CPT2 and CPT1 gene expression in the liver of fetuses and offspring at weaning age. In conclusion, maternal high-fat diet can impair gene expression involved in FAO in the placenta by downregulating the AMPK signaling pathway, and can cause glucose and lipid dysfunction of offspring at weaning, indicating that placental FAO may play a crucial role in regulating maternal overnutrition and metabolic health in the offspring.

Dataset Information

Relation of placental alkaline phosphatase expression in human term placenta with maternal and offspring fat mass.

Publications

Relation of placental alkaline phosphatase expression in human term placenta with maternal and offspring fat mass.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets