Adiposopathy
Open accessAbstract
Being overweight or obese is a worldwide epidemic. Adiposity can cause fat mass-related cardiovascular disease (CVD). Adiposity may also cause adipocyte and adipose tissue anatomic and functional abnormalities, termed adiposopathy (adipose-opathy) or "sick fat," that result in endocrine and immune derangements. Adiposopathy may directly contribute to CVD through pericardiac and perivascular effects on the myocardium and blood vessels. Adiposopathy may also indirectly contribute to CVD through promoting or worsening major CVD risk factors such as type 2 diabetes mellitus, high blood pressure, and dyslipidemia. Despite CVD being the most common cause of mortality among overweight individuals, the pathophysiologic relationship between adiposity and CVD is often thought mysterious, as evidenced by "obesity paradoxes." Underlying this uncertainty are suggestions that excessive body fat does not always increase the risk of CVD and, in some cases, may actually decrease such risks. These paradoxical findings are made less paradoxical when the pathogenic potential of excessive body fat is assessed based on adipose tissue dysfunction rather than simply on increased fat mass alone. This introductory review 1) provides a brief historical perspective of the pathogenic potential of adipose tissue; 2) describes the relationships between adipose tissue (histology, embryology, and adipogenesis) and cardiovascular medicine; 3) outlines the anatomic, functional, endocrine, and immune manifestations of adiposopathy; and 4) describes the importance of cross talk and/or interactions of adipose tissue with other body tissues. Finally, this review describes how "sick fat" helps account for various clinical obesity/cardiovascular paradoxes, supporting adiposopathy as a cardiovascular disease.
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Excess adiposity increases CVD risk directly through negative effects on the endocrine and immune systems and indirectly through obesity-related complications including type 2 diabetes, hypertension, dyslipidaemia, thrombosis or sleep disorders.
“with excess adiposity increasing the risk of CVD directly through negative effects on the endocrine and immune systems,3,4 and indirectly through the development of obesity-related complications, including type 2 diabetes (T2D), hypertension, dyslipidaemia, thrombosis or sleep disorders, which are CVD risk factors.3”
From Tirzepatide compared with semaglutide and 10-year cardiovascular disease risk reduction in obesity: <i>post-hoc</i> analysis of the SURMOUNT-5 trial (2025) · cites this paper as [4]
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- Authors
- Bays, H. E.
- Affiliations
- Louisville Metabolic and Atherosclerosis Research Center (US)
- Corresponding author
- Bays, Harold E.
- ORCID
- Bays, Harold E.
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 57
- Issue
- 25
- Pages
- 2461-2473
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W52052328
- Cited by
- 431
- References
- 17
- Citations by year
- 2026: 14 · 2025: 37 · 2024: 28 · 2023: 30 · 2022: 40 · 2021: 26 · 2020: 24 · 2019: 27 · 2018: 29 · 2017: 21 · 2016: 22 · 2015: 26 · 2014: 36 · 2013: 34 · 2012: 30
- FWCI
- 23.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- adiposopathy, obesity, adipose tissue dysfunction, cardiovascular disease, adipogenesis, adipose tissue endocrine function, obesity paradox, type 2 diabetes, dyslipidemia, hypertension
- MeSH terms
- Cardiovascular Diseases, Endocrine System Diseases, Humans, Obesity, Adiposity
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