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Metabolites
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Metabolites in Cardio-Metabolic Disease: Unravelling New Markers and Mechanisms
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Metabolites in Cardio-Metabolic Disease: Unravelling New Markers and Mechanisms

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (30 November 2019) | Viewed by 8027

Special Issue Editors

Prof. Dr. Gemma Figtree

E-Mail Website
Guest Editor
Northern Clinical School, Kolling Institute of Medical Research, Faculty of Medicine and Health, St Leonards, Australia
Interests: coronary atherosclerosis; inflammation and oxidative stress in the heart and blood vessel; Clinical trials
Special Issues, Collections and Topics in MDPI journals
Dr. John O'Sullivan

E-Mail Website
Guest Editor
Charles Perkins Centre, Camperdown, The University of Sydney, Sydney 2006, Australia
Interests: metabolites; cardiac metabolism; atherosclerosis; heart failure; diabetes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent developments in technology platforms—including nuclear magnetic resonance spectroscopy and mass spectrometry—combined with advances in computational bioinformatics, provide opportunities for unravelling completely unexpected mechanisms and new markers of disease risk. Such approaches are ideal tools for breakthrough discoveries in complex diseases typified by atherosclerosis, cardiomyopathy, and metabolic syndrome. Here we call for manuscripts addressing the current challenges of, and exploring opportunities for, the application of metabolomic studies in the cardiovascular field.

The Special Issue will cover recent advances and methodological limitations, as well as the clinical implications. Reviews and perspectives as well as original data are welcome.

Dr. John O'Sullivan
Prof. Dr. Gemma Figtree
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiovascular
  • metabolites
  • multi-omics
  • bioinformatics
  • personalized medicine
  • biomarker

Published Papers (2 papers)

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Research

11 pages, 951 KiB  
Article
Possible Use of Blood Tryptophan Metabolites as Biomarkers for Coronary Heart Disease in Sudden Unexpected Death
by Kobchai Santisukwongchote, Yutti Amornlertwatana, Thanapat Sastraruji and Churdsak Jaikang
Metabolites 2020, 10(1), 6; https://doi.org/10.3390/metabo10010006 - 19 Dec 2019
Cited by 6 | Viewed by 2845
Abstract
Coronary heart disease (CHD) is the major cause of death in sudden unexpected death (SUD) cases. Tryptophan (TRP) and its metabolites are correlated with the CHD patient but less studies in the SUD. The aim of this study was to evaluate the relationship [...] Read more.
Coronary heart disease (CHD) is the major cause of death in sudden unexpected death (SUD) cases. Tryptophan (TRP) and its metabolites are correlated with the CHD patient but less studies in the SUD. The aim of this study was to evaluate the relationship of TRP and its metabolites with the CHD in the SUD cases. Blood samples and heart tissues were collected from CHD subjects (n = 31) and the control group (n = 72). Levels of kynurenine (KYN), kynurenic acid (KYA), xanthurenic acid (XAN), 3-hydroxyanthranillic acid (HAA), quinolinic acid (QA), picolinic acid (PA) and 5-hydroxyindoleacetic acid (HIAA) were determined by HPLC-DAD. A severity of heart occlusion was categorized into four groups, and the relationship was measured with the TRP metabolites. The HIAA and The KYN levels significantly differed (p < 0.01) between the CHD group and the control group. Lower levels of QA/XAN, PA/KA, HAA/XAN, KYN/XAN and KYN/TRP were found in the CHD group. However, PA/HAA, PA/HIAA, PA/KYN and XAN/KA values in the CHD group were higher than the control group (p < 0.05). This study revealed that the values of PA/KA and PA/HAA provided better choices for a CHD biomarker in postmortem bodies. Full article
(This article belongs to the Special Issue Metabolites in Cardio-Metabolic Disease: Unravelling New Markers and Mechanisms)
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22 pages, 4168 KiB  
Article
Barth Syndrome: Exploring Cardiac Metabolism with Induced Pluripotent Stem Cell-Derived Cardiomyocytes
by Erica M. Fatica, Gina A. DeLeonibus, Alisha House, Jillian V. Kodger, Ryan W. Pearce, Rohan R. Shah, Liraz Levi and Yana Sandlers
Metabolites 2019, 9(12), 306; https://doi.org/10.3390/metabo9120306 - 17 Dec 2019
Cited by 16 | Viewed by 4831
Abstract
Barth syndrome (BTHS) is an X-linked recessive multisystem disorder caused by mutations in the TAZ gene (TAZ, G 4.5, OMIM 300394) that encodes for the acyltransferase tafazzin. This protein is highly expressed in the heart and plays a significant role in cardiolipin biosynthesis. [...] Read more.
Barth syndrome (BTHS) is an X-linked recessive multisystem disorder caused by mutations in the TAZ gene (TAZ, G 4.5, OMIM 300394) that encodes for the acyltransferase tafazzin. This protein is highly expressed in the heart and plays a significant role in cardiolipin biosynthesis. Heart disease is the major clinical manifestation of BTHS with a high incidence in early life. Although the genetic basis of BTHS and tetralinoleoyl cardiolipin deficiency in BTHS-affected individuals are well-established, downstream metabolic changes in cardiac metabolism are still uncovered. Our study aimed to characterize TAZ-induced metabolic perturbations in the heart. Control (PGP1-TAZWT) and TAZ mutant (PGP1-TAZ517delG) iPS-CM were incubated with 13C6-glucose and 13C5-glutamine and incorporation of 13C into downstream Krebs cycle intermediates was traced. Our data reveal that TAZ517delG induces accumulation of cellular long chain acylcarnitines and overexpression of fatty acid binding protein (FABP4). We also demonstrate that TAZ517delG induces metabolic alterations in pathways related to energy production as reflected by high glucose uptake, an increase in glycolytic lactate production and a decrease in palmitate uptake. Moreover, despite mitochondrial dysfunction, in the absence of glucose and fatty acids, TAZ517delG-iPS-CM can use glutamine as a carbon source to replenish the Krebs cycle. Full article
(This article belongs to the Special Issue Metabolites in Cardio-Metabolic Disease: Unravelling New Markers and Mechanisms)
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