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Regulation of visceral and epicardial adipose tissue for preventing cardiovascular injuries associated to obesity and diabetes
Open accessAbstract
Nowadays, obesity is seriously increasing in most of the populations all over the world, and is associated with the development and progression of high-mortality diseases such as type-2 diabetes mellitus (T2DM) and its subsequent cardiovascular pathologies. Recent data suggest that both body fat distribution and adipocyte phenotype, can be more determinant for fatal outcomes in obese patients than increased general adiposity. In particular, visceral adiposity is significantly linked to long term alterations on different cardiac structures, and in developed forms of myocardial diseases such as hypertensive and ischaemic heart diseases, and diabetic cardiomyopathy. Interestingly, this depot may be also related to epicardial fat accumulation through secretion of lipids, adipokines, and pro-inflammatory and oxidative factors from adipocytes. Thus, visceral adiposity and its white single-lipid-like adipocytes, are risk factors for different forms of heart disease and heart failure, mainly in higher degree obese subjects. However, under specific stimuli, some of these adipocytes can transdifferentiate to brown multi-mitochondrial-like adipocytes with anti-inflammatory and anti-apoptotic proprieties. Accordingly, in order to improve potential cardiovascular abnormalities in obese and T2DM patients, several therapeutic strategies have been addressed to modulate the visceral and epicardial fat volume and phenotypes. In addition to lifestyle modifications, specific genetic manipulations in adipose tissue and administration of PPARγ agonists or statins, have improved fat volume and phenotype, and cardiovascular failures. Furthermore, incretin stimulation reduced visceral and epicardial fat thickness whereas increased formation of brown adipocytes, alleviating insulin resistance and associated cardiovascular pathologies.
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“More specifically, treatments ameliorating the altered composition and distribution of fat stores may produce the best results [117].”
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 [117]
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“Recent data suggest that both body fat distribution and adipocyte phenotype are more likely to increase fatal outcomes in obese patients than a higher general adiposity [2].”
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“[36] found that VAT may also be associated with epicardial fat accumulation by secreting lipids, fat factors, and proinflammatory and oxidative factors from adipocytes.”
BackgroundCannabis and Myocardial Infarction: Risk Factors and Pathogenetic Insights.
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“Therefore, we designed the present study to evaluate and compare these two parameters, along with other CVD risk factors in patients with RA.”
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Adiponectin inhibits D‑gal‑induced cardiomyocyte senescence via AdipoR1/APPL1
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Role of Distinct Fat Depots in Metabolic Regulation and Pathological Implications
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Mitochondrial Homeostasis Mediates Lipotoxicity in the Failing Myocardium
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“At the other end of the spectrum, decreased VAT has been associated with a reduction in CVD risk [23].”
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“Subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) play distinct roles in predicting the risk of cardiovascular complications in diabetes [20, 21].”
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“Numerous cohort studies have shown that VFA, rather than SFA, is closely related to diabetes and cardiovascular events [18, 19].”
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BackgroundTargeting obesity for therapeutic intervention in heart failure patients
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“In addition to these anatomical effects, EAP is involved in the development and progression of HFpEF through its metabolic effects [46].”
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Relationship between adipose tissue distribution and arterial stiffness in HFpEF
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Metadata
- Authors
- González, N., Moreno-Villegas, Z., González-Bris, A., Egido, J., & Lorenzo, Ó.
- Affiliations
- Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas (ES)
- Hospital Universitario Fundación Jiménez Díaz (ES)
- Corresponding author
- Lorenzo, Ó.
- Venue
- Cardiovascular Diabetology
- Published
- 2017-04-04
- Volume
- 16
- Issue
- 1
- Pages
- 44-44
- ISSN
- 1475-2840 (ISSN-L)
- PMC
- PMC5379721
- OpenAlex
- W2604392184
- Cited by
- 211
- References
- 124
- Citations by year
- 2026: 15 · 2025: 12 · 2024: 28 · 2023: 14 · 2022: 29 · 2021: 30 · 2020: 29 · 2019: 22 · 2018: 24 · 2017: 5
- FWCI
- 3.08
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Cardiovascular Diabetology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Banco de Santander-Universidad Autónoma (CEAL-AL/2015-17)
- Esteve Laboratories (2017)
- ISCarlos III (PI14/00386, PIE13/00051)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- visceral adipose tissue, epicardial adipose tissue, obesity, type 2 diabetes, cardiovascular disease, diabetic cardiomyopathy, adipocyte phenotype, brown adipocytes, adipokines, PPARγ agonists, statins, incretin-based therapy, insulin resistance, heart failure, body fat distribution
- MeSH terms
- Adipose Tissue, Adipose Tissue, Brown, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Humans, Obesity, Pericardium, Intra-Abdominal Fat, Incretins
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