Epicardial adipocyte size does not correlate with body mass index

Aitken‐Buck, Hamish M.; Babakr, Aram A; Coffey, Sean; Jones, Peter P.; Tse, Rexson; Lamberts, Regis R.

doi:10.1016/j.carpath.2019.07.003

Cited by 11 publications

(7 citation statements)

References 21 publications

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“…In contrast, EAT adipocyte morphology has a less defined relationship with BMI. Although early work seemed to suggest that mean EAT adipocyte size increased slightly with BMI in lean, overweight, and obese post-mortem cases [18], recent intra-individual post-mortem analyses from our group found that unlike adipocytes from other SAT and VAT depots, EAT adipocyte size does not correlate with BMI [19].…”

Section: Introductioncontrasting

confidence: 68%

“…Our data suggest that not only does EAT adipocyte size not change with BMI, but that EAT adipocyte size does not change in parallel with increased EAT deposition (Figure 2(c)). Recent work from our group, and earlier work from other labs, has found that EAT adipocyte size does not correlate with BMI in post-mortem cases or cardiac surgery patients [19,29]. Thus, our current study suggests that increased EAT thickness that is associated with increased BMI does not occur by hypertrophy of the constituent adipocytes, as has been reported as the predominant mechanism of expansion in other fat depots.…”

Section: Adipose Tissue and Adipocyte Size Relationshipsupporting

confidence: 58%

“…We have recently reported that the size of adipocytes comprising the EAT of 43 post-mortem cases have no association with BMI, neither when stratified into BMI categories nor when analysed using Pearson correlation [19]. We aimed to corroborate these results in patients undergoing cardiac surgery in the current study.…”

Section: Eat Adipocyte Size and Bmi Relationshipmentioning

confidence: 71%

“…Unfortunately, quantification of EAT deposition was not accessible for our previous study [19]. Therefore, for the current study, we utilized echocardiographic EAT thickness measured in cardiac surgery patients and assessed the relationship between the EAT thickness and the size of the adipocytes comprising the fat tissue.…”

Section: Introductionmentioning

confidence: 99%

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Relationship between epicardial adipose tissue thickness and epicardial adipocyte size with increasing body mass index

et al. 2019

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Macroscopic deposition of epicardial adipose tissue (EAT) has been strongly associated with numerous indices of obesity and cardiovascular disease risk. In contrast, the morphology of EAT adipocytes has rarely been investigated. We aimed to determine whether obesity-driven adipocyte hypertrophy, which is characteristic of other visceral fat depots, is found within EAT adipocytes. EAT samples were collected from cardiac surgery patients (n = 49), stained with haematoxylin & eosin, and analysed for mean adipocyte size and non-adipocyte area. EAT thickness was measured using echocardiography. A significant positive relationship was found between EAT thickness and body mass index (BMI). When stratified into standardized BMI categories, EAT thickness was 58.7% greater (p = 0.003) in patients from the obese (7.3 ± 1.8 mm) compared to normal (4.6 ± 0.9 mm) category. BMI as a continuous variable significantly correlated with EAT thickness (r = 0.56, p < 0.0001). Conversely, no correlation was observed between adipocyte size and either BMI or EAT thickness. No difference in the nonadipocyte area was found between BMI groups. Our results suggest that the increased macroscopic EAT deposition associated with obesity is not caused by adipocyte hypertrophy. Rather, alternative remodelling via adipocyte proliferation might be responsible for the observed EAT expansion. ARTICLE HISTORY

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Section: Introductioncontrasting

confidence: 68%

Section: Adipose Tissue and Adipocyte Size Relationshipsupporting

confidence: 58%

Section: Eat Adipocyte Size and Bmi Relationshipmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

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Relationship between epicardial adipose tissue thickness and epicardial adipocyte size with increasing body mass index

et al. 2019

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“…In addition to perivascular fat deposits which appear to protect the coronary vasculature [ 61 ], epicardial adipose tissue also covers large stretches of the ventricular epicardium in healthy individuals [ 58 ]. The extent and thickness of the epicardial adipose tissue increases as body–mass index increases through over-weight and obese in larger mammals such as humans [ 60 , 62 ]. Both obesity and increased epicardial adipose tissue volume/thickness are risk factors for cardiovascular disease including atrial fibrillation [ 51 , 63 , 64 ].…”

Section: Epicardial Adipose Tissue Fibrosis and Atrial Fibrillationmentioning

confidence: 99%

Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?

Krishnan

Chilton

Raman

et al. 2021

Cells

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Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts depolarized when coupled myocytes produced action potentials. This review also introduces another non-myocyte which may modulate both myocardial (myo)fibroblasts and myocytes: epicardial adipose tissue. Epicardial adipocytes are in intimate contact with myocytes and (myo)fibroblasts and may infiltrate the myocardium. Adipocytes secrete numerous adipokines which modulate (myo)fibroblast and myocyte physiology. These adipokines are protective in healthy hearts, preventing inflammation and fibrosis. However, adipokines secreted from adipocytes may switch to pro-inflammatory and pro-fibrotic, associated with reactive oxygen species generation. Pro-fibrotic adipokines stimulate myofibroblast differentiation, causing pronounced fibrosis in the epicardial adipose tissue and the myocardium. Adipose tissue also influences myocyte electrophysiology, via the adipokines and/or through electrotonic interactions. Deeper understanding of the interactions between myocytes and non-myocytes is important to understand and manage atrial fibrillation.

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Association of epicardial adipose tissue volume with heart weight in post-mortem cases

Aitken-Buck,

Moore,

Bingham

et al. 2024

Forensic Sci Med Pathol

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Epicardial adipose tissue (EAT) deposition has been long associated with heart weight. However, recent research has failed to replicate this association. We aimed to determine the association of EAT volume with heart weight in post-mortem cases and identify potential confounding variables. EAT volume derived from post-mortem computed tomography (PMCT) and heart weight were measured in post-mortem cases (N = 87, age: 56 ± 16 years, 28% female). Cases with hypertrophied heart weights (N = 44) were determined from reference tables. Univariable associations were tested using Spearman correlation and simple linear regression. Independence was determined with stepwise regression. In the total cohort, EAT volume (median 66 ± 45 cm3) was positively associated with heart weight (median 435 ± 132 g) at the univariable level (r = 0.6, P < 0.0001) and after adjustment for age, female sex, and various body size metrics (R2 adjusted = 0.41–0.57). Median EAT volume was 1.9-fold greater in cases with hypertrophic hearts (P < 0.0001) but with considerably greater variability, especially in cases with extreme EAT volume or heart weight. As such, EAT volume was not associated with heart weight in hypertrophic cases, while a robust independent association was found in non-hypertrophic cases (R2 adjusted = 0.62–0.86). EAT mass estimated from EAT volume found that EAT comprised approximately 13% of overall heart mass in the total cases. This was significantly greater in cases with hypertrophy (median 15.5%; range, 3.6–36.6%) relative to non-hypertrophied cases (12.5%, 3.3–24.3%) (P = 0.04). EAT volume is independently and positively associated with heart weight in post-mortem cases. Excessive heart weight significantly confounded this association.

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Epicardial adipocyte size does not correlate with body mass index

Cited by 11 publications

References 21 publications

Relationship between epicardial adipose tissue thickness and epicardial adipocyte size with increasing body mass index

Relationship between epicardial adipose tissue thickness and epicardial adipocyte size with increasing body mass index

Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?

Association of epicardial adipose tissue volume with heart weight in post-mortem cases

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