Summary of Study ST003274

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.

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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 IDST003274
Study TitleMetabolomics 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 water soluble metabolites within healthy and human heart failure conditions with a focus on ischaemic cardiomyopathy with diabetes and is part of a project which also integrates lipidomics, 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 Date2024-05-05
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:SU003394
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
SA35449499Donor F
SA35449592Donor F
SA354496111Donor F
SA354497109Donor F
SA35449894Donor F
SA35449996Donor F
SA354500105Donor F
SA354501103Donor F
SA354502101Donor F
SA35450398Donor F
SA35450493Donor M
SA35450595Donor M
SA35450697Donor M
SA354507102Donor M
SA354508100Donor M
SA354509106Donor M
SA354510107Donor M
SA354511108Donor M
SA354512110Donor M
SA35451391Donor M
SA3545143ICM-DM F
SA3545152ICM-DM M
SA3545161ICM-DM M
SA3545176ICM-DM M
SA3545184ICM-DM M
SA35451914ICM-DM M
SA35452013ICM-DM M
SA35452112ICM-DM M
SA35452211ICM-DM M
SA35452310ICM-DM M
SA3545249ICM-DM M
SA3545258ICM-DM M
SA3545267ICM-DM M
SA3545275ICM-DM M
SA35452819ICM-No DM F
SA35452917ICM-No DM F
SA35453016ICM-No DM F
SA35453126ICM-No DM F
SA35453220ICM-No DM F
SA35453321ICM-No DM F
SA35453427ICM-No DM F
SA35453524ICM-No DM M
SA35453630ICM-No DM M
SA35453722ICM-No DM M
SA35453823ICM-No DM M
SA35453918ICM-No DM M
SA35454028ICM-No DM M
SA35454129ICM-No DM M
SA35454215ICM-No DM M
SA35454325ICM-No DM M
SA35454439NICM-DM F
SA35454532NICM-DM F
SA35454638NICM-DM F
SA35454731NICM-DM F
SA35454833NICM-DM M
SA35454934NICM-DM M
SA35455035NICM-DM M
SA35455136NICM-DM M
SA35455237NICM-DM M
SA35455340NICM-No DM F
SA35455446NICM-No DM F
SA35455554NICM-No DM F
SA35455652NICM-No DM F
SA35455744NICM-No DM F
SA35455856NICM-No DM M
SA35455941NICM-No DM M
SA354560104NICM-No DM M
SA35456142NICM-No DM M
SA35456243NICM-No DM M
SA35456347NICM-No DM M
SA35456445NICM-No DM M
SA35456555NICM-No DM M
SA35456648NICM-No DM M
SA35456749NICM-No DM M
SA35456850NICM-No DM M
SA35456953NICM-No DM M
SA35457051NICM-No DM M
Showing results 1 to 77 of 77

Collection:

Collection ID:CO003387
Collection Summary:Donated human myocardium. Refer to uploaded acquisition methods.
Collection Protocol Filename:IHD-DM_paper_metabolomics_methods.pdf
Sample Type:Heart
Storage Conditions:Described in summary

Treatment:

Treatment ID:TR003403
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_metabolomics_methods.pdf

Sample Preparation:

Sampleprep ID:SP003401
Sampleprep Summary:Refer to the uploaded methods file.
Sampleprep Protocol Filename:IHD-DM_paper_metabolomics_methods.pdf

Chromatography:

Chromatography ID:CH004061
Chromatography Summary:HPLC gradient: The HPLC gradient program begins with an initial condition of 5% solvent A and 95% solvent B, with a flow rate of 0.25 mL/min, which is held for 0.5 minutes to establish system equilibration. The gradient then proceeds as follows: at 6 minutes, the mobile phase composition shifts to 60% solvent A and 40% solvent B for 3minutes; at 10 minutes, it changes back to 5% solvent A and 95% solvent B; at 11 minutes, the flow rate increases to 0.4 mL/min while maintaining a composition of 5% solvent A and 95% solvent B for a duration of 12.5 minutes; and at 24.5 minutes, the flow rate decreases back to 0.25 mL/min. The final condition is maintained for 1 minutes to ensure stability before subsequent analyses.
Methods Filename:IHD-DM_paper_HPLC_settings.pdf
Instrument Name:Agilent 1260
Column Name:Waters Atlantis HILIC (150 x 2.1mm,3um)
Column Temperature:40°C
Flow Gradient:The HPLC gradient program begins with an initial condition of 5% solvent A and 95% solvent B, with a flow rate of 0.25 mL/min, which is held for 0.5 minutes to establish system equilibration. The gradient then proceeds as follows: at 6 minutes, the mobile phase composition shifts to 60% solvent A and 40% solvent B for 3minutes; at 10 minutes, it changes back to 5% solvent A and 95% solvent B; at 11 minutes, the flow rate increases to 0.4 mL/min while maintaining a composition of 5% solvent A and 95% solvent B for a duration of 12.5 minutes; and at 24.5 minutes, the flow rate decreases back to 0.25 mL/min.
Flow Rate:0.250 – 0.400 mL/min
Solvent A:100% water; 0.1% formic acid; 10 mM ammonium Formate (pH ~2.5)
Solvent B:100% acetonitrile; 0.1% formic acid
Chromatography Type:HILIC
  
Chromatography ID:CH004062
Chromatography Summary:HPLC gradient: The HPLC gradient program is initialized with an initial mobile phase composition of 15% solvent A and 85% solvent B at a flow rate of 0.25 mL/min. Over the course of 8 minutes, the mobile phase composition undergoes a transition to 65% solvent A and 35% solvent B. Subsequently, at 8 minutes, the composition shifts to 98% solvent A and 2% solvent B, maintained for 1 minute. The mobile phase reverts back to the initial composition of 15% solvent A and 85% solvent B at 10 minutes. At 12.5 minutes, the flow rate is increased to 0.5 mL/min, while maintaining a constant mobile phase composition of 15% solvent A and 85% solvent B for a period of 2.5 minutes. Finally, at 15 minutes, the flow rate is reduced back to 0.25 mL/min. To ensure system stability, the final condition is maintained for 1 minute prior to subsequent analyses.
Methods Filename:IHD-DM_paper_HPLC_settings.pdf
Instrument Name:Agilent 1260
Column Name:Waters XBridge Amide (100 x 2.1mm,3.5um)
Column Temperature:40°C
Flow Gradient:The HPLC gradient program is initialized with an initial mobile phase composition of 15% solvent A and 85% solvent B at a flow rate of 0.25 mL/min. Over the course of 8 minutes, the mobile phase composition undergoes a transition to 65% solvent A and 35% solvent B. Subsequently, at 8 minutes, the composition shifts to 98% solvent A and 2% solvent B, maintained for 1 minute. The mobile phase reverts back to the initial composition of 15% solvent A and 85% solvent B at 10 minutes. At 12.5 minutes, the flow rate is increased to 0.5 mL/min, while maintaining a constant mobile phase composition of 15% solvent A and 85% solvent B for a period of 2.5 minutes.
Flow Rate:0.250 – 0.400 mL/min
Solvent A:95% water/5% acetonitrile; 20mM ammonium acetate; 20mM ammonium hydroxide (pH 9.0)
Solvent B:100% acetonitrile
Chromatography Type:HILIC

Analysis:

Analysis ID:AN005360
Analysis Type:MS
Analysis Protocol File:IHD-DM_paper_metabolomics_methods.pdf
Chromatography ID:CH004061
Num Factors:10
Num Metabolites:81
Units:Relative abundance.
  
Analysis ID:AN005361
Analysis Type:MS
Analysis Protocol File:IHD-DM_paper_metabolomics_methods.pdf
Chromatography ID:CH004062
Num Factors:10
Num Metabolites:73
Units:Relative abundance.
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