Fuel availability and fate in cardiac metabolism: a tale of two substrates

Pascual, Florencia; Coleman, Rosalind A.

doi:10.1016/j.bbalip.2016.03.014

Cited by 125Cardiovascular Function and Risk FactorsCardiac Ischemia and ReperfusionMitochondrial Function and Pathology

Fuel availability and fate in cardiac metabolism: a tale of two substrates

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Pascual, Florencia, Coleman, Rosalind A.·2016·Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids

DOI 10.1016/j.bbalip.2016.03.014PMC PMC4983230

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Abstract

The heart's extraordinary metabolic flexibility allows it to adapt to normal changes in physiology in order to preserve its function. Alterations in the metabolic profile of the heart have also been attributed to pathological conditions such as ischemia and hypertrophy; however, research during the past decade has established that cardiac metabolic adaptations can precede the onset of pathologies. It is therefore critical to understand how changes in cardiac substrate availability and use trigger events that ultimately result in heart dysfunction. This review examines the mechanisms by which the heart obtains fuels from the circulation or from mobilization of intracellular stores. We next describe experimental models that exhibit either an increase in glucose use or a decrease in FA oxidation, and how these aberrant conditions affect cardiac metabolism and function. Finally, we highlight the importance of alternative, relatively under-investigated strategies for the treatment of heart failure. This article is part of a Special Issue entitled: Heart Lipid Metabolism edited by G.D. Lopaschuk.

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Obesity can cause metabolic inflexibility of the heart and alter substrate selection.
“Obesity can cause metabolic inflexibility of the heart and alter substrate selection (179).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [179]

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Cardiometabolism as an Interlocking Puzzle between the Healthy and Diseased Heart: New Frontiers in Therapeutic Applications
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Ceramide-1-phosphate alleviates high-altitude pulmonary edema by stabilizing circadian ARNTL-mediated mitochondrial dynamics
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Therapeutic Potential of VEGF-B in Coronary Heart Disease and Heart Failure: Dream or Vision?
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Citri Reticulatae Pericarpium protects against isoproterenol-induced chronic heart failure via activation of PPARγ
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Molecular and cellular mechanisms in diabetic heart failure: Potential therapeutic targets
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Glucose Transporter Expression and Regulation Following a Fast in the Ruby-throated Hummingbird, Archilochus colubris
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The alpha-1A adrenergic receptor agonist A61603 reduces cardiac polyunsaturated fatty acid and endocannabinoid metabolites associated with inflammation in vivo
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Metabolic Crosstalk between the Heart and Fat
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Mitochondria at the Heart of Sepsis: Mechanisms, Metabolism, and Sex Differences
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Omics Technologies in Personalized Combination Therapy for Cardiovascular Diseases: Challenges and Opportunities
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Ultrafast Ultrasound Imaging for Super-Resolution Preclinical Cardiac PET
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Maternal high fat–high energy diet alters metabolic factors in the non‐human primate fetal heart
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What causes cardiac mitochondrial failure at high environmental temperatures?
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The Bitter Side of Sugar Consumption: A Mitochondrial Perspective on Diabetes Development
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Whole-Exome Sequencing and hiPSC Cardiomyocyte Models Identify MYRIP, TRAPPC11, and SLC27A6 of Potential Importance to Left Ventricular Hypertrophy in an African Ancestry Population
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Metabolic Response of the Immature Right Ventricle to Acute Pressure Overloading
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Integrated multi-omics mapping of mitochondrial dysfunction and substrate preference in Barth syndrome cardiac tissue
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Adipose Lipolysis Regulates Cardiac Glucose Uptake and Function in Mice under Cold Stress
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Parkinson’s Disease and the Heart: Studying Cardiac Metabolism in the 6-Hydroxydopamine Model
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13C NMR of glutamate for monitoring the pentose phosphate pathway in myocardium
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Dietary Mg2+ Intake and the Na+/Mg2+ Exchanger SLC41A1 Influence Components of Mitochondrial Energetics in Murine Cardiomyocytes
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Authors: Pascual, F., & Coleman, R. A.
Affiliations: University of North Carolina at Chapel Hill (US)
Corresponding author: Coleman, Rosalind A.
ORCID: Pascual, Florencia
Coleman, Rosalind A.
Venue: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
Publisher: Elsevier BV
Published: 2016-10
Volume: 1861
Issue: 10
Pages: 1425-1433
ISSN: 1388-1981 (ISSN-L)
DOI: 10.1016/j.bbalip.2016.03.014
PMC: PMC4983230
OpenAlex: W2301336672
Cited by: 125
References: 159
Citations by year: 2026: 15 · 2025: 14 · 2024: 11 · 2023: 12 · 2022: 11 · 2021: 24 · 2020: 15 · 2019: 5 · 2018: 8 · 2017: 6 · 2016: 3
FWCI: 1.28
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
UNC Libraries
Funders: National Institutes of Health (DK56599, DK59935)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: myocardial metabolism, metabolic flexibility, glucose utilization, fatty acid oxidation, substrate availability, myocardial ischemia, cardiac hypertrophy, heart failure, heart failure treatment
MeSH terms: Animals, Energy Metabolism, Fatty Acids, Glucose, Humans, Myocardium, Oxidation-Reduction, Substrate Specificity

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