Summary of Study ST001448

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000995. The data can be accessed directly via it's Project DOI: 10.21228/M8311J This work is supported by NIH grant, U2C- DK119886.

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Study IDST001448
Study TitleMaternal Hypercortisolemia alters placental metabolism: NMR metabolomics
Study SummaryNMR metabolomic studies of placental tissue from sheep with excess maternal cortisol during late gestation
Institute
University of Florida
Last NameWalejko
First NameJacquelyn
Address300 N Duke St Durham NC 27701
Emailjacquelyn.walejko@duke.edu
Phone9194792304
Submit Date2020-08-18
Raw Data AvailableYes
Raw Data File Type(s)fid
Analysis Type DetailNMR
Release Date2020-09-16
Release Version1
Jacquelyn Walejko Jacquelyn Walejko
https://dx.doi.org/10.21228/M8311J
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000995
Project DOI:doi: 10.21228/M8311J
Project Title:Maternal Hypercortisolemia alters placental metabolism
Project Summary:Previous studies have suggested that increases in maternal cortisol or maternal stress in late pregnancy increase the risk of stillbirth at term. In an ovine model with increased maternal cortisol over the last 0.20 of gestation, we have previously found evidence of disruption of fetal serum and cardiac metabolomics, and altered expression of genes related to mitochondrial function and metabolism in biceps femoris, diaphragm and cardiac muscle. The present studies were designed to test for effects of chronically increased maternal cortisol on gene expression and metabolomics in placentomes near term. We hypothesized that changes in placenta may underlie or contribute to the alterations in fetal serum metabolomics, and thereby contribute to changes in striated muscle metabolism. Placentomes were collected from pregnancies in early labor (143±1 d gestation) of control ewes (n=7) or ewes treated with cortisol (1 mg/kg/d iv; n=5) starting at day 115 of gestation. Transcriptomics and metabolomics were performed using an ovine gene expression microarray (Agilent 019921) and HR-MAS NMR, respectively. Multi-omic analysis indicates that amino acid metabolism, particularly of branched chain amino acids and glutamate occur in placenta; changes in amino acid metabolism, degradation or biosynthesis in placenta were consistent with changes in valine, isoleucine, leucine and glycine in fetal serum. The analysis also indicates changes in glycerophospholipid metabolism and suggests changes in ER stress and antioxidant status in the placenta. These findings suggest that changes in placental function occurring with excess maternal cortisol in late gestation may contribute to metabolic dysfunction at birth.
Institute:University of Florida
Department:Pharmacodynamics
Last Name:Keller-Wood
First Name:Maureen
Address:1345 SW Archer Rd, PO 100487, Gainesville, FL 32610
Email:kellerwd@cop.ufl.edu
Phone:352-273-7687

Subject:

Subject ID:SU001522
Subject Type:Mammal
Subject Species:Ovis aries
Taxonomy ID:9940

Factors:

Subject type: Mammal; Subject species: Ovis aries (Factor headings shown in green)

mb_sample_id local_sample_id Treatment Sex
SA123772749Control Female
SA123773993BControl Female
SA123774568Control Female
SA123775594Control Male
SA123776993AControl Male
SA123777784Control Male
SA123778521Control Male
SA123779713Cortisol Female
SA123780768Cortisol Female
SA123781665Cortisol Female
SA123782656Cortisol Female
SA123783874Cortisol Female
Showing results 1 to 12 of 12

Collection:

Collection ID:CO001517
Collection Summary:Placentomes were collected at necropsy from control ewes and ewes treated with cortisol (CORT: 1mg/kg/d from day 115 of pregnancy) at days 141-144 of gestation. CORT ewes received an intravenous infusion of cortisol (Solu-Cortef, hydrocortisone sodium succinate in sodium phosphate; Pfizer, New York, NY); control animals did not receive any treatment. Animals were sacrificed for collection of tissues at the first signs of labor, as evidenced by changes in uterine blood flow; placentomes were collected from sheep in early stages of labor at between 141-144 days and 142-144 days of gestation in the cortisol-treated and control groups, respectively. In this cohort of ewes, there were 7 control ewes, of which data were collected from placentomes of 7 live fetuses (including one set of twins); there was one lamb born, and that placenta was not collected. In this cohort there were 11 cortisol- treated ewes, from which we collected placentomes from 5 live fetuses. There was one live lamb born, and 5 stillborn lambs, from which placentas were not collected. Placentomes were classified as A-D placentomes, snap frozen in liquid nitrogen, and stored in -80C until metabolomic analysis.
Sample Type:Placenta

Treatment:

Treatment ID:TR001537
Treatment Summary:Placentomes were collected at necropsy from control ewes and ewes treated with cortisol (CORT: 1mg/kg/d from day 115 of pregnancy) at days 141-144 of gestation. CORT ewes received an intravenous infusion of cortisol (Solu-Cortef, hydrocortisone sodium succinate in sodium phosphate; Pfizer, New York, NY); control animals did not receive any treatment.

Sample Preparation:

Sampleprep ID:SP001530
Sampleprep Summary:High-resolution magic angle spinning (HR-MAS) proton nuclear magnetic resonance (1H-NMR) was used to determine metabolites present in placental tissue. Briefly, 30 μL of deuterium oxide (D2O) with 3.3 mM 3-(Trimethylsilyl)-1-propanesulfonic acid (DSS) as a reference standard was added to 27.7-52.1 mg (mean 35.3 mg) of placental tissue before being placed into a 4 mm HR-MAS rotor (Bruker Biospin) and spun at 6 kHz with a spectral width of 10 ppm. Data were acquired on an Avance III 600 MHz Bruker NMR spectrometer equipped with a 4 mm HR-MAS probe at the University of Georgia Complex Carbohydrate Research Center. Data were acquired using a one-dimensional experiment with T2 filter using Carr-Purcell-Meiboom-Gill (CPMG) pulse sequence with water presaturation (CPMGPR1D).

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