Summary of Study ST003275

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 PR002031. The data can be accessed directly via it's Project DOI: 10.21228/M83529 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.

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Study IDST003275
Study TitleLipidomics analysis within healthy donors and end-stage heart failure with a focus on ischaemic cardiomyopathy with diabetes
Study TypeHuman heart failure left ventricular myocardial metabolomics study across multiple disease phenotypes.
Study SummaryThis study involves the analysis of lipids within healthy and human heart failure conditions with a focus on ischaemic cardiomyopathy with diabetes and is part of a project which also integrates metabolomics, proteomics, RNA-seq, and histological analyses to identify molecular mechanisms influencing disease phenotypes. Ischaemic cardiomyopathy (ICM) is the most common cause of heart failure (HF) and often coexists with diabetes mellitus (DM). Yet, their combined effects are seldom investigated and are poorly understood. Herein, we performed multi-omic analyses of end-stage ICM with DM (ICM-DM) against ICM-No DM, non-ischaemic (dilated) cardiomyopathy with DM (NICM-DM), NICM-No DM, and healthy age-matched donors (AMD). Tissue was sourced from pre-mortem human left ventricular myocardium. Though fatty acid oxidation (FAO) proteins were down-regulated in ICM-DM relative to AMD and other HF, the unique ICM-DM down-regulation of acylcarnitines, perilipin, and ketone body, amino acid, and glucose metabolising proteins indicated FAO may not be entirely impaired. Oxidative phosphorylation appeared reduced in HF but exacerbated in ICM-DM, consistent with purportedly increased oxidative stress. Extracellular matrix proteins including collagens were up-regulated principally in ICM-DM despite the absence of macroscopic scar tissue. These findings were supported histologically and in metabolomic and RNA sequencing analyses.
Institute
University of Sydney
Last NameHunter
First NameBenjamin
AddressJohn Hopkins Dr, Camperdown, NSW, 2006, Australia
Emailbenjamin.hunter@sydney.edu.au
Phone+61422525639
Submit Date2024-05-26
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2025-05-06
Release Version1
Benjamin Hunter Benjamin Hunter
https://dx.doi.org/10.21228/M83529
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:

Project:

Project ID:PR002031
Project DOI:doi: 10.21228/M83529
Project Title:Diabetic ischaemic cardiomyopathy: Characterising the left ventricular myocardial molecular profile in advanced human heart failure
Project Type:Human heart failure left ventricular myocardial multi-omics study across multiple disease phenotypes
Project Summary:Ischaemic cardiomyopathy (ICM) is the most common cause of heart failure (HF) and often coexists with diabetes mellitus (DM). Yet, their combined effects are seldom investigated and are poorly understood. Herein, we performed multi-omic analyses of end-stage ICM with DM (ICM-DM) against ICM-No DM, non-ischaemic (dilated) cardiomyopathy with DM (NICM-DM), NICM-No DM, and healthy age-matched donors (AMD). Tissue was sourced from pre-mortem human left ventricular myocardium. Though fatty acid oxidation (FAO) proteins were down-regulated in ICM-DM relative to AMD and other HF, the unique ICM-DM down-regulation of acylcarnitines, perilipin, and ketone body, amino acid, and glucose metabolising proteins indicated FAO may not be entirely impaired. Oxidative phosphorylation appeared reduced in HF but exacerbated in ICM-DM, consistent with purportedly increased oxidative stress. Extracellular matrix proteins including collagens were up-regulated principally in ICM-DM despite the absence of macroscopic scar tissue. These findings were supported histologically and in metabolomic and RNA sequencing analyses.
Institute:The University of Sydney
Last Name:Hunter
First Name:Benjamin
Address:John Hopkins Dr, Camperdown, NSW, 2006, Australia
Email:benjamin.hunter@sydney.edu.au
Phone:+61422525639

Subject:

Subject ID:SU003395
Subject Type:Human
Subject Species:Homo sapiens
Taxonomy ID:9606
Age Or Age Range:21-66 years
Gender:Male and female
Species Group:Mammals

Factors:

Subject type: Human; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Condition Sex
SA35457194Donor F
SA35457287Donor F
SA354573105Donor F
SA354574103Donor F
SA35457589Donor F
SA35457691Donor F
SA35457799Donor F
SA35457898Donor F
SA35457993Donor F
SA35458088Donor M
SA35458190Donor M
SA35458292Donor M
SA35458397Donor M
SA35458495Donor M
SA354585100Donor M
SA354586101Donor M
SA354587102Donor M
SA354588104Donor M
SA35458986Donor M
SA3545903ICM-DM F
SA3545912ICM-DM M
SA3545921ICM-DM M
SA35459310ICM-DM M
SA3545947ICM-DM M
SA35459513ICM-DM M
SA35459612ICM-DM M
SA35459711ICM-DM M
SA3545989ICM-DM M
SA3545998ICM-DM M
SA3546006ICM-DM M
SA3546015ICM-DM M
SA3546024ICM-DM M
SA35460314ICM-DM M
SA35460416ICM-No DM F
SA35460519ICM-No DM F
SA35460620ICM-No DM F
SA35460721ICM-No DM F
SA35460817ICM-No DM F
SA35460927ICM-No DM F
SA35461026ICM-No DM F
SA35461118ICM-No DM M
SA35461224ICM-No DM M
SA35461315ICM-No DM M
SA35461423ICM-No DM M
SA35461522ICM-No DM M
SA35461630ICM-No DM M
SA35461729ICM-No DM M
SA35461828ICM-No DM M
SA35461925ICM-No DM M
SA35462039NICM-DM F
SA35462131NICM-DM F
SA35462232NICM-DM F
SA35462338NICM-DM F
SA35462433NICM-DM M
SA35462534NICM-DM M
SA35462635NICM-DM M
SA35462736NICM-DM M
SA35462837NICM-DM M
SA35462952NICM-No DM F
SA35463040NICM-No DM F
SA35463154NICM-No DM F
SA35463246NICM-No DM F
SA35463344NICM-No DM F
SA35463443NICM-No DM M
SA35463541NICM-No DM M
SA35463642NICM-No DM M
SA35463753NICM-No DM M
SA35463845NICM-No DM M
SA35463947NICM-No DM M
SA35464048NICM-No DM M
SA35464149NICM-No DM M
SA35464251NICM-No DM M
SA35464356NICM-No DM M
SA35464455NICM-No DM M
SA35464550NICM-No DM M
Showing results 1 to 75 of 75

Collection:

Collection ID:CO003388
Collection Summary:Donated human myocardium. Refer to uploaded acquisition methods.
Collection Protocol Filename:IHD-DM_paper_lipidomics_methods
Sample Type:Heart
Storage Conditions:Described in summary

Treatment:

Treatment ID:TR003404
Treatment Summary:Non-diseased/healthy donor left ventricular human myocardial tissue was compared the left ventricle of heart failure phenotypes; ischaemic cardiomyopathy with diabetes (ICM-DM), ischaemic cardiomyopathy without diabetes (ICM-No DM), non-ischaemic cardiomyopathy with diabetes (NICM-DM), and non-ischaemic cardiomyopathy without diabetes (NICM-No DM).
Treatment Protocol Filename:IHD-DM_paper_lipidomics_methods

Sample Preparation:

Sampleprep ID:SP003402
Sampleprep Summary:Refer to the uploaded methods file.
Sampleprep Protocol Filename:IHD-DM_paper_lipidomics_methods

Chromatography:

Chromatography ID:CH004063
Methods Filename:IHD-DM_paper_lipidomics_methods
Instrument Name:Thermo Vanquish
Column Name:Waters ACQUITY UPLC CSH C18 (100 x 2.1mm,1.7um)
Column Temperature:45°C
Flow Gradient:0 min, 80:20 A/B; 3 min, 80:20 A/B; 5.5 min, 55:45 A/B; 8 min, 36:65 A/B; 13 min, 15:85 A/B; 14 min, 0:100 A/B; 20 min, 0:100 A/B; 20.2 min, 70:30 A/B; 27 min, 70:30 A/B
Flow Rate:0.28 mL/min
Solvent A:60% acetonitrile/40% water; 0.1% formic acid; 10 mM ammonium formate
Solvent B:90% isopropanol/10% acetonitrile; 0.1% formic acid; 10 mM ammonium formate
Chromatography Type:Reversed phase

Analysis:

Analysis ID:AN005362
Analysis Type:MS
Analysis Protocol File:IHD-DM_paper_lipidomics_methods
Chromatography ID:CH004063
Num Factors:10
Num Metabolites:216
Units:nmoles/mg tissue
  
Analysis ID:AN005363
Analysis Type:MS
Analysis Protocol File:IHD-DM_paper_lipidomics_methods
Chromatography ID:CH004063
Num Factors:10
Num Metabolites:138
Units:nmoles/mg tissue
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