Nutrient sensing and utilization: getting to the heart of metabolic flexibility
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A central feature of obesity-related cardiometabolic diseases is the impaired ability to transition between fatty acid and glucose metabolism. This impairment, referred to as "metabolic inflexibility", occurs in a number of tissues, including the heart. Although the heart normally prefers to metabolize fatty acids over glucose, the inability to upregulate glucose metabolism under energetically demanding conditions contributes to a pathological state involving energy imbalance, impaired contractility, and post-translational protein modifications. This review discusses pathophysiologic processes that contribute to cardiac metabolic inflexibility and speculates on the potential physiologic origins that lead to the current state of cardiometabolic disease in an obesogenic environment.
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Acetylation of mitochondrial proteins propagates metabolic inflexibility and deacetylation promotes metabolic flexibility.
“Acetylation of mitochondrial proteins propagates metabolic inflexibility and deacetylation promotes metabolic flexibility (178, 259).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [178]
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“This impairment is known as “metabolic inflexibility” (Griffin et al., 2015), that is present in obese people since they are able to oxidize lipids in insulin-stimulated conditions instead to metabolize glucose being mitochondria the key organelles affecting this incapacity (Storlien et al., 2004).”
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Enhancing mitochondrial pyruvate metabolism ameliorates myocardial ischemic reperfusion injuryPreprint
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- Authors
- Griffin, T. M., Humphries, K. M., Kinter, M., Lim, H.-Y., & Szweda, L. I.
- Affiliations
- Oklahoma Medical Research Foundation (US)
- Corresponding author
- Griffin, Timothy M.
- Venue
- Biochimie
- Publisher
- Elsevier BV
- Published
- 2016-05
- Volume
- 124
- Pages
- 74-83
- ISSN
- 0037-9042 (ISSN-L)
- 0300-9084
- PMC
- PMC4828282
- OpenAlex
- W1752066541
- Cited by
- 36
- References
- 123
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 3 · 2019: 4 · 2018: 7 · 2017: 6 · 2016: 4
- FWCI
- 0.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochimie (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (P20GM103441, P20GM104934, P20GM103636)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R03AR066828)
- National Institute on Aging (R01AG049058)
- American Heart Association (14GRNT20510031, 13SDG14680005)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- metabolic flexibility, nutrient sensing, glucose metabolism, fatty acid metabolism, obesity, cardiometabolic disease, heart contractility, post-translational protein modification, energy imbalance
- MeSH terms
- Animals, Energy Metabolism, Glucose, Heart Diseases, Humans, Myocardial Contraction, Myocardium, Obesity, Protein Processing, Post-Translational
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