Summary of project PR000995
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.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| 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 |
Summary of all studies in project PR000995
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST001448 | Maternal Hypercortisolemia alters placental metabolism: NMR metabolomics | Ovis aries | University of Florida | - | 2020-09-16 | 1 | 12 | Uploaded data (4.4M)* |
