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Adaptation and Maladaptation of the Heart in Obesity
Open accessAbstract
O besity appears to be a major cause of hypertension and associated cardiovascular pathophysiology, including cardiac dysfunction.However, obesity may lead to abnormal cardiac function through mechanisms that are independent of, or that act in concert with, hypertension.One hypothesis of obesity-induced cardiac dysfunction is that an oversupply of substrates leads first to adaptive changes and eventually to contractile dysfunction of the heart.We reason that increased supply of nonesterified fatty acids, together with metabolic dysregulation in obesity, including an inadequate activation of fat oxidation, results in the accumulation of toxic lipid byproducts and subsequent contractile dysfunction.Although the phenomenon may have already been known to Virchow 1 when he described "fatty metamorphosis" of the heart, the concept of cardiac "lipotoxicity" re-emerged only recently with its description in the heart of the obese Zucker diabetic fatty rat. 2 The concept is, however, still a hypothesis rather than an established physiological principle.In spite of the many investigations performed in rodent models, the mechanism(s) responsible for impaired contractile function of the heart is still obscure, and it is uncertain whether lipid metabolites contribute to "obesity cardiomyopathy" in humans.Our brief review is an attempt to understand the chronic regulatory effects of changes in systemic metabolism on cardiac function.In other words, we discuss current concepts of cardiac adaptation and maladaptation to a deranged metabolic environment.
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“Obesity is closely associated with cardiac disorders, which is assumed to be a consequence of the adaption to an oversupply of high-fat substrates [262,263].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [262]
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Metadata
- Authors
- Harmancey, R., Wilson, C. R., & Taegtmeyer, H.
- Affiliations
- Texas Medical Center (US)
- Venue
- Hypertension
- Published
- 2008-08
- Volume
- 52
- Issue
- 2
- Pages
- 181-187
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- PMC
- PMC3660087
- OpenAlex
- W2137438717
- Cited by
- 121
- References
- 100
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 5 · 2022: 11 · 2021: 3 · 2020: 3 · 2019: 3 · 2018: 6 · 2017: 3 · 2016: 9 · 2015: 8 · 2014: 13 · 2013: 4 · 2012: 10
- FWCI
- 1.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL061483, R01HL073162)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- obesity, obesity cardiomyopathy, cardiac dysfunction, lipotoxicity, free fatty acids, fat oxidation, lipid accumulation, contractile dysfunction, cardiac adaptation, metabolic dysfunction, Zucker diabetic fatty rats
- MeSH terms
- Adaptation, Physiological, Animals, Disease Models, Animal, Fatty Acids, Nonesterified, Female, Heart Failure, Humans, Male, Myocardial Contraction, Myocardium, Obesity, Morbid, Prognosis, Severity of Illness Index, Cohort Studies, Body Mass Index, Reactive Oxygen Species, Risk Assessment, Mice
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