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Fetal macrosomia in a Hispanic/Latinx predominant cohort and altered expressions of genes related to placental lipid transport and metabolism.

ABSTRACT: INTRODUCTION:Fetal overgrowth, termed fetal macrosomia when birth weight is >4000?g, is the major concern in the treatment of gestational diabetes mellitus (GDM). However, to date, the underlying mechanisms of fetal macrosomia have not been understood completely. Placental lipid metabolism is emerging as a critical player in fetal growth. In this study, we hypothesized that fatty-acid transport and metabolism in the placental tissue is impaired in GDM women, dependent on fetal sex. METHODS:To test this hypothesis, we analyzed the incidence of GDM, fetal macrosomia, and obesity in a large cohort consisting of 17,995 pregnant subjects and majority of subjects being Hispanic/Latinx, and investigated expression of genes related to lipid transport and metabolism in placentas from obese women with or without GDM, and with or without fetal macrosomia. RESULTS:The main findings include: (1) there was a higher incidence of GDM and obesity in Hispanic subjects compared with non-Hispanic subjects, but not fetal macrosomia; (2) expressions of most of genes related to placental lipid transport and metabolism were not altered by the presence of GDM, fetal macrosomia, or fetal sex; (3) expression of FABP4 was increased in obese women with GDM and fetal macrosomia, and this occurred in male placentas; (4) expression of LPL was decreased in obese women with GDM despite fetal macrosomia, and this occurred in male placentas; (5) expression of ANGPTL3 was decreased in obese women with GDM and fetal macrosomia, but was not altered when fetal sex was included in the analysis. CONCLUSIONS:This study indicates that there is race disparity in GDM with higher incidence of GDM in obese Hispanic women, although fetal macrosomia disparity is not present. Moreover, altered placental lipid transport may contribute to fetal overgrowth in obese women with GDM.

SUBMITTER: Yang H

PROVIDER: S-EPMC7387181 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Fetal macrosomia in a Hispanic/Latinx predominant cohort and altered expressions of genes related to placental lipid transport and metabolism.

Yang Heqin H He Bin B Yallampalli Chandra C Gao Haijun H

International journal of obesity (2005) 20200603 8

<h4>Introduction</h4>Fetal overgrowth, termed fetal macrosomia when birth weight is >4000 g, is the major concern in the treatment of gestational diabetes mellitus (GDM). However, to date, the underlying mechanisms of fetal macrosomia have not been understood completely. Placental lipid metabolism is emerging as a critical player in fetal growth. In this study, we hypothesized that fatty-acid transport and metabolism in the placental tissue is impaired in GDM women, dependent on fetal sex.<h4>Me ...[more]

PMID: 32494035

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Project description:BackgroundWorldwide, stillbirth is one of the leading causes of death. Altered fetal growth and placental abnormalities are the strongest and most prevalent known risk factors for stillbirth. The aim of this study was to identify patterns of association between placental abnormalities, fetal growth, and stillbirth.Methods and findingsPopulation-based case-control study of all stillbirths and a representative sample of live births in 59 hospitals in 5 geographic areas in the U.S. Fetal growth abnormalities were categorized as small (<10th percentile) and large (>90th percentile) for gestational age at death (stillbirth) or delivery (live birth) using a published algorithm. Placental examination by perinatal pathologists was performed using a standardized protocol. Data were weighted to account for the sampling design. Among 319 singleton stillbirths and 1119 singleton live births at ?24 weeks at death or delivery respectively, 25 placental findings were investigated. Fifteen findings were significantly associated with stillbirth. Ten of the 15 were also associated with fetal growth abnormalities (single umbilical artery; velamentous insertion; terminal villous immaturity; retroplacental hematoma; parenchymal infarction; intraparenchymal thrombus; avascular villi; placental edema; placental weight; ratio birth weight/placental weight) while 5 of the 15 associated with stillbirth were not associated with fetal growth abnormalities (acute chorioamnionitis of placental membranes; acute chorioamionitis of chorionic plate; chorionic plate vascular degenerative changes; perivillous, intervillous fibrin, fibrinoid deposition; fetal vascular thrombi in the chorionic plate). Five patterns were observed: placental findings associated with (1) stillbirth but not fetal growth abnormalities; (2) fetal growth abnormalities in stillbirths only; (3) fetal growth abnormalities in live births only; (4) fetal growth abnormalities in stillbirths and live births in a similar manner; (5) a different pattern of fetal growth abnormalities in stillbirths and live births.ConclusionsThe patterns of association between placental abnormalities, fetal growth, and stillbirth provide insights into the mechanism of impaired placental function and stillbirth. They also suggest implications for clinical care, especially for placental findings amenable to prenatal diagnosis using ultrasound that may be associated with term stillbirths.

Dataset Information

Fetal macrosomia in a Hispanic/Latinx predominant cohort and altered expressions of genes related to placental lipid transport and metabolism.

Publications

Fetal macrosomia in a Hispanic/Latinx predominant cohort and altered expressions of genes related to placental lipid transport and metabolism.

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