Summary of Study ST002254

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 PR001442. The data can be accessed directly via it's Project DOI: 10.21228/M8B71S 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.

Perform statistical analysis  |  Show all samples  |  Show named metabolites  |  Download named metabolite data  
Download mwTab file (text)   |  Download mwTab file(JSON)   |  Download data files (Contains raw data)
Study IDST002254
Study TitleMaternal obesity alters offspring liver and skeletal muscle metabolism in early post-puberty despite maintaining a normal post-weaning dietary lifestyle
Study SummaryMaternal obesity (MO) during pregnancy is linked to increased and premature risk of age-related metabolic diseases in the offspring. However, the underlying molecular mechanisms still remain not fully understood. Using a well-established baboon model of MO, we analyzed tissue biopsies and plasma samples obtained from post-pubertal offspring (3-6.5y at sample collection) of MO mothers (n=19) and from control animals born to mothers fed a standard diet (CON, n=13). All offspring ate normal chow diet after weaning. With an untargeted gas chromatography-mass spectrometry metabolomics profiling, we quantified a total of 351 liver, 316 skeletal muscle and 423 plasma metabolites. We found 58 metabolites significantly altered in liver and 46 in skeletal muscle of MO offspring, including 8 metabolites shared between both tissues. Male and female-specific metabolites in opposite direction of change were found in liver and skeletal muscle of MO offspring. Several tissue-specific and 4 shared metabolic pathways were identified from these dysregulated metabolites. Interestingly, none of the tissue-specific metabolic alterations reflected in plasma. Our results identify tissue metabolites and pathways in post-pubertal MO offspring in a sex-specific manner.
Institute
Wake Forest School of Medicine
Last NameAmpong
First NameIsaac
AddressCenter for Precision Medicine, Department of Internal Medicine, Section on Molecular Medicine, Wake Forest University, Winston-Salem, North Carolina, United States
Emailiampong@wakehealth.edu
Phone3367162091
Submit Date2022-08-02
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailGC-MS
Release Date2022-08-31
Release Version1
Isaac Ampong Isaac Ampong
https://dx.doi.org/10.21228/M8B71S
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:


Sample Preparation:

Sampleprep ID:SP002346
Sampleprep Summary:15 μL of plasma, liver or skeletal muscle samples were subjected to sequential solvent extraction, once each with 1 mL of acetonitrile: isopropanol: water (3:3:2) and 500 μL of acetonitrile: water (1:1) mixtures at 4°C [14]. An internal standard, adonitol (2 μL from 10 mg/ml stock) was added to each aliquot prior to the extraction. The extracts were dried under vacuum at 4°C prior to chemical derivatization (silylation reactions). Blank tubes without samples, were treated similarly as sample tubes and added to account for background noise and other sources of contamination. Samples and blanks were sequentially derivatized with meth-oxyamine hydrochloride (MeOX) and 1% TMCS in N-methyl-N-trimethylsilyl-trifluoroacetamide (MSTFA) or 1% TMCS containing N-(t-butyldimethylsilyl)-N-methyltrifluoroacetamide (MTBSTFA) as described elsewhere [15]. Briefly, the steps involved addition of 20 μL of MeOX (20 mg mL-1) in pyridine incu-bated at 55°C for 60 min followed by trimethylsilylation at 60°C for 60 min after adding 80 μL MTBSTFA.
  logo