Summary of Study ST002797
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 PR001745. The data can be accessed directly via it's Project DOI: 10.21228/M8513X This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST002797 |
| Study Title | Fetal metabolic adaptations to cardiovascular stress in twin-twin transfusion syndrome |
| Study Summary | Monochorionic-diamniotic twin pregnancies comprise 70% of identical twin pregnancies and are susceptible to unique complications arising from a single placenta shared by two fetuses. Twin-twin transfusion syndrome (TTTS) is a constellation of disturbances caused by unequal blood flow within the shared placenta giving rise to a major hemodynamic imbalance between the twins. If untreated, it leads to fetal cardiac failure and death. Here, we applied TTTS as a model to uncover fetal metabolic adaptations to cardiovascular stress. We compared untargeted mass spectrometry-based metabolomic analyses of amniotic fluid samples from a cohort of severe TTTS cases showing sonographic evidence of increased afterload and heart failure vs. uncomplicated singleton controls. Amniotic fluid metabolites demonstrated footprints of changes in fatty acid, glucose, and steroid hormone metabolism in TTTS. Among TTTS cases, unsupervised principal component analysis revealed two distinct clusters of disease defined by levels of glucose metabolites, amino acids, urea, and redox status. Our results suggest that the human fetal heart can adapt to hemodynamic stress by modulating its glucose metabolism. Furthermore, we have uncovered heterogeneity among cases of severe TTTS suggesting potential differences in the ability of individual fetuses to respond to cardiovascular stress. |
| Institute | University of Texas Health Science Center at Houston |
| Last Name | Parchem |
| First Name | Jacqueline |
| Address | 6431 Fannin, MSB 3.286 |
| jacqueline.g.parchem@uth.tmc.edu | |
| Phone | 415-250-6257 |
| Submit Date | 2023-07-01 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | mzdata.xml |
| Analysis Type Detail | LC-MS |
| Release Date | 2023-08-15 |
| Release Version | 1 |
Select appropriate tab below to view additional metadata details:
Project:
| Project ID: | PR001745 |
| Project DOI: | doi: 10.21228/M8513X |
| Project Title: | Amniotic fluid metabolites in TTTS |
| Project Summary: | Monochorionic-diamniotic twin pregnancies comprise 70% of identical twin pregnancies and are susceptible to unique complications arising from a single placenta shared by two fetuses. Twin-twin transfusion syndrome (TTTS) is a constellation of disturbances caused by unequal blood flow within the shared placenta giving rise to a major hemodynamic imbalance between the twins. If untreated, it leads to fetal cardiac failure and death. Here, we applied TTTS as a model to uncover fetal metabolic adaptations to cardiovascular stress. We compared untargeted mass spectrometry-based metabolomic analyses of amniotic fluid samples from a cohort of severe TTTS cases showing sonographic evidence of increased afterload and heart failure vs. uncomplicated singleton controls. Amniotic fluid metabolites demonstrated footprints of changes in fatty acid, glucose, and steroid hormone metabolism in TTTS. Among TTTS cases, unsupervised principal component analysis revealed two distinct clusters of disease defined by levels of glucose metabolites, amino acids, urea, and redox status. Our results suggest that the human fetal heart can adapt to hemodynamic stress by modulating its glucose metabolism. Furthermore, we have uncovered heterogeneity among cases of severe TTTS suggesting potential differences in the ability of individual fetuses to respond to cardiovascular stress. |
| Institute: | The University of Texas Health Science Center at Houston |
| Last Name: | Parchem |
| First Name: | Jacqueline |
| Address: | 6431 Fannin, MSB 3.286, Houston, TX, 77030, USA |
| Email: | jacqueline.g.parchem@uth.tmc.edu |
| Phone: | 415-250-6257 |
Subject:
| Subject ID: | SU002904 |
| Subject Type: | Human |
| Subject Species: | Homo sapiens |
| Taxonomy ID: | 9606 |
| Species Group: | Mammals |
Factors:
Subject type: Human; Subject species: Homo sapiens (Factor headings shown in green)
| mb_sample_id | local_sample_id | Group |
|---|---|---|
| SA300454 | C1_160 | Control |
| SA300455 | C9_213 | Control |
| SA300456 | C10_215 | Control |
| SA300457 | C2_171 | Control |
| SA300458 | C7_190 | Control |
| SA300459 | C8_194 | Control |
| SA300460 | C6_190 | Control |
| SA300461 | C4_186 | Control |
| SA300462 | C3_183 | Control |
| SA300463 | C5_189 | Control |
| SA300464 | T17_281D | TTTS |
| SA300465 | T16_262D | TTTS |
| SA300466 | T15_258D | TTTS |
| SA300467 | T14_253R | TTTS |
| SA300468 | T13_231R | TTTS |
| SA300469 | T22_421D | TTTS |
| SA300470 | T21_360R | TTTS |
| SA300471 | T20_322R | TTTS |
| SA300472 | T19_317R | TTTS |
| SA300473 | T18_287D | TTTS |
| SA300474 | T7_121DR | TTTS |
| SA300475 | T4_109R | TTTS |
| SA300476 | T3_106DR | TTTS |
| SA300477 | T2_52D | TTTS |
| SA300478 | T1_48D | TTTS |
| SA300479 | T5_114R | TTTS |
| SA300480 | T6_118DR | TTTS |
| SA300481 | T11_181R | TTTS |
| SA300482 | T10_175R | TTTS |
| SA300483 | T9_164D | TTTS |
| SA300484 | T8_161R | TTTS |
| SA300485 | T12_184R | TTTS |
| Showing results 1 to 32 of 32 |
Collection:
| Collection ID: | CO002897 |
| Collection Summary: | Amniotic fluid was previously collected and banked from pregnant individuals with monochorionic-diamniotic twins complicated by TTTS undergoing fetoscopic laser ablation of placental anastomoses at the UTHealth Houston Fetal Center at Children’s Memorial Hermann Hospital. Samples were collected from the recipient twin sac immediately upon entry with the operative cannula and prior to placental laser ablation or amnioinfusion for improving the visualization. The amniotic fluid was centrifuged, and the supernatant was stored at -80 C for future use. Frozen genetic amniocentesis samples, discarded from further analyses, served as controls. For TTTS cases, demographics, clinical characteristics, and outcomes were abstracted from the Fetal Center research database which is maintained by trained research staff. For controls, available clinical variables were limited to maternal age, gestational age, indication for amniocentesis, and genetic testing results. |
| Sample Type: | Amniotic fluid |
Treatment:
| Treatment ID: | TR002913 |
| Treatment Summary: | not applicable |
Sample Preparation:
| Sampleprep ID: | SP002910 |
| Sampleprep Summary: | Amniotic fluid metabolites were extracted by addition of 1 part amniotic fluid to 15 parts 70% acetonitrile in ddH2O (vol:vol). The mixture was briefly vortexed and then centrifuged for 5 min at 16,000 × g to pellet precipitated proteins. The protein pellet was solubilized in 0.2M NaOH and quantified by DC Protein Assay (Bio-Rad). The volume of metabolite extract was normalized by amniotic protein content. |
Chromatography:
| Chromatography ID: | CH003419 |
| Instrument Name: | Agilent 6550 QTOF |
| Column Name: | MicroSolv Diamond Hydride (150 x 2.1mm, 4um) |
| Column Temperature: | 25 |
| Flow Gradient: | 0-1.0 min, 99% B; 1.0-15.0 min, to 20% B; 15.0 to 29.0, 0% B; 29.1 to 37min, 99% B |
| Flow Rate: | 0.4 mL/min |
| Solvent A: | 50% isopropanol/50% water; 0.025% acetic acid |
| Solvent B: | 90% acetonitrile/10% water; 5 mM ammonium acetate |
| Chromatography Type: | Normal phase |
Analysis:
| Analysis ID: | AN004550 |
| Analysis Type: | MS |
| Chromatography ID: | CH003419 |
| Num Factors: | 2 |
| Num Metabolites: | 165 |
| Rt Units: | Minutes |
| Units: | intensity |
| Analysis ID: | AN004551 |
| Analysis Type: | MS |
| Chromatography ID: | CH003419 |
| Num Factors: | 2 |
| Num Metabolites: | 155 |
| Rt Units: | Minutes |
| Units: | intensity |