Epicardial adipose tissue feeding and overfeeding the heart
Abstract
Epicardial adipose tissue is a particular visceral fat depot with unique anatomic, biomolecular, and genetic features. Epicardial fat displays both physiological and pathological properties. Epicardial fat expresses genes and secretes cytokines actively involved in the thermogenesis and regulation of lipid and glucose metabolism of the adjacent myocardium. A disequilibrium between epicardial fat feeding and overfeeding the myocardium with free fatty acids leads to intramyocardial fat infiltration causing organ damage and clinical consequences. The upregulation of epicardial fat proinflammatory and lipogenic genes contributes to the fat build up in the proximal coronary arteries. Epicardial fat is a measurable and modifiable risk factor that can serve as a novel and additional tool for cardiovascular risk stratification. Pharmacologically targeting epicardial fat with drugs such as glucagon peptide-like 1 analogs or sodium glucose transport 2 inhibitors reduces the epicardial fat burden and induces beneficial cardiometabolic effects. Assessment and manipulation of epicardial fat transcriptome might open new avenues in the prevention of cardiometabolic diseases.
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An enlarged and biologically transformed EAT loses its physiological protective role and acquires lipotoxic effects through excess FFA release, leading to abnormal lipid deposition and fatty infiltration in the myocardium.
“This is what can happen when an enlarged and biologically transformed EAT coats the heart, thus losing its physiological protective role, and acquiring lipotoxic effects throughout an excess FFa release, which leads to abnormal lipid deposition and fatty infiltration in the myocardium [52].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [52]
High-FA feeding of the heart by EAT may lead to intramyocardial fat accumulation causing functional derangements.
“Similarly, a high-FA feeding of the heart by EAT may lead to intramyocardial fat accumulation causing functional derangements [52].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [52]
In systemic disorders such as T2DM and obesity, the adipocytes within the epicardium take on the features of white adipose tissue, overfilled with lipids and prone to lipolysis, releasing an excess of FAs.
“In systemic disorders such as T2DM and obesity, the adipocytes within the epicardium take on the features of white adipose tissue (WAT), namely they are overfilled with lipids and prone to lipolysis, releasing an excess of FAs [52].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [52]
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References 66 · Cited by 82
- Authors
- Iacobellis, G., & Barbaro, G.
- Affiliations
- University of Miami (US)
- Corresponding author
- Iacobellis, Gianluca
- ORCID
- Iacobellis, Gianluca
- Venue
- Nutrition
- Publisher
- Elsevier BV
- Published
- 2019-03
- Volume
- 59
- Pages
- 1-6
- ISSN
- 0899-9007 (ISSN-L)
- OpenAlex
- W2883200109
- Cited by
- 82
- References
- 66
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 6 · 2023: 11 · 2022: 14 · 2021: 13 · 2020: 13 · 2019: 6
- FWCI
- 1.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- epicardial adipose tissue, myocardial fatty acid uptake, coronary artery disease, pro-inflammatory genes, lipogenic genes, thermogenesis, myocardial glucose metabolism, cardiovascular risk stratification, GLP-1 receptor agonists, SGLT2 inhibitors, cardiometabolic disease
- MeSH terms
- Adipose Tissue, Coronary Artery Disease, Glucose, Humans, Myocardium, Pericardium, Risk Factors, Cytokines, Thermogenesis, Lipid Metabolism
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