Adiponectin expression in human epicardial adipose tissue in vivo is lower in patients with coronary artery disease

Iacobellis, Gianluca; Pistilli, Daniela; Gucciardo, Marco; Leonetti, Frida; Miraldi, Fabio; Brancaccio, Gianluca; Gallo, Pietro; Gioia, Cira Di

doi:10.1016/j.cyto.2004.11.002

Cited by 286 publications

(324 citation statements)

References 24 publications

Supporting

Mentioning

299

Contrasting

Unclassified

Order By: Relevance

“…This finding is justified according to the common embryogenesis pathway; that is, epicardial fat and intra-abdominal fat seem to be originally brown adipose tissue in infancy. This adipose depot is now recognized as a source of variable bioactive molecules, such as adiponectin (Iacobellis et al 2005b), tumor necrosis factoralfa, monocyte chemotactic factor-1, interleukine-1 beta, interleukine-6 (Mazurek et al 2003) and inflammatory cytokines which might affect coronary artery (Hirata et al 2011a(Hirata et al , 2011b. In fact, some epicardial fat-related cytokines, such as adiponectin, resistin, and free fatty acids, have been linked to hypertension, coronary artery disease, endothelial dysfunction, and sympathetic over activity (Bruun et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Increased Epicardial Adipose Tissue Thickness Is Correlated with Ascending Aortic Diameter

Çanğa

Kocaman

Çetin

et al. 2012

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Epicardial adipose tissue (EAT), localized beneath the visceral pericardium, is a metabolically active endocrine and paracrine organ with possible interactions within the heart. Recent studies identified possible roles of uric acid (UA)-induced oxidative stress and increased inflammatory status in the pathogenesis of ascending aortic dilatation. The aim of this study was to investigate whether EAT is an independent factor for ascending aortic dilatation. The patients were evaluated by a complete transthoracic echocardiographic examination including measurements of EAT and aortic dimensions. Serum levels of UA and C-reactive protein and EAT thicknesses were compared in 38 patients with dilated ascending aorta (DAA) (the diameter ≥ 37 mm) vs. 107 subjects with normal aortic diameter (AD) of < 37 mm. EAT thickness was significantly higher in DAA group compared to normal AD group (8.3 ± 2.7 vs. 5.4 ± 2.2 mm, p < 0.001) as well as age (53 ± 10 vs. 48 ± 9 years, p = 0.004), the presence of hypertension (54% vs. 30%, p = 0.009) and UA levels (6.0 ± 1.4 vs. 5.2 ± 1.1 mg/dL, p < 0.001). There was a strong correlation between EAT thickness and ascending aortic diameter (r = 0.521, p < 0.001). In multiple logistic regression analysis, EAT thickness (OR: 1.429, p = 0.006), body mass index (OR: 1.169, p = 0.014) and UA levels (OR: 1.727, p = 0.023) were independently correlated to ascending aortic dilatation. We therefore propose that increased EAT thickness is an independent predictor of ascending aortic dilation.

show abstract

Section: Discussionmentioning

confidence: 99%

Increased Epicardial Adipose Tissue Thickness Is Correlated with Ascending Aortic Diameter

Çanğa

Kocaman

Çetin

et al. 2012

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

show abstract

“…5,[18][19][20][21][22][23] Iacobellis, et al reported that mRNA expression of adiponectin in epicardial adipose tissue was significantly lower in subjects with severe CAD than in those without CAD. 21) Our data suggest that enhanced infiltration of inflammatory cells into EAT may account for inflammatory cytokine expression in EAT of CAD patients, although our sample size was too small to draw a definitive conclusion. Further investigation is needed to clarify the influence of adipokines on the formation of atherosclerotic lesions and inflammation in epicardial adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Inflammation in Epicardial Fat in Patients With Coronary Artery Disease

et al. 2011

View full text Add to dashboard Cite

SummaryIt has been hypothesized that epicardial fat, a local visceral fat depot with close proximity to coronary arteries, may serve as a source of inflammatory cytokines and cells in coronary atherosclerotic lesions. Here, we characterized infiltration of inflammatory cells and expression of adipocytokines in epicardial adipose tissue in patients with and without coronary artery disease (CAD). Pare samples were obtained from epicardial and subcutaneous adipose tissue during elective cardiac surgery (CAD, n = 8; non-CAD, n = 9). Inflammatory cell infiltration was investigated by immunohistochemical staining using antibodies against CD3, CD4, CD8 and CD68. Expression of adipocytokines was evaluated by real-time quantitative reverse transcription-polymerase chain reaction. Infiltration of macrophages and CD8-positive T cells in the epicardial adipose tissue in the CAD group was greater than that in the non-CAD group. In contrast, there was no significant difference between the two groups in the number of inflammatory cells in subcutaneous adipose tissue. No statistical difference could be found between the CAD group and the non-CAD group in the expression levels of adiponectin and inflammatory cytokines in epicardial adipose tissue. Our findings suggest that inflammatory cell infiltration is enhanced in epicardial adipose tissue, but not in subcutaneous fat, in patients with coronary artery disease. Chronic inflammation in epicardial fat may influence the pathogenesis of coronary atherosclerosis. (Int Heart J 2011; 52: 139-142)

show abstract

“…In recent years, attention has focused on the role of visceral adipose tissue due to the synthesis and release of a number of adipokines from adipocytes [12][13][14]. In MetS, increased visceral adipose tissue disturbs adipokine secretion and leads to a low-grade chronic inflammatory state mediated by the infiltration of macrophages into adipose tissue [14].…”

Section: Abdominal Obesity and Adipokine Imbalancementioning

confidence: 99%

“…This inflammatory state is found to be associated with IR [15][16][17] and with atherosclerosis [14]. Visceral adipose tissue functions as a paracrine and an endocrine organ, secreting a number of adipokines, some of which are proinflammatory and atherogenic, such as leptin, tumor necrosis factor-α (TNF-α), resistin, interleukin-6 (IL-6), and fatty acid-binding protein 4, and others, which have anti-inflammatory, protective effects such as adiponectin [12,13]. In MetS patients, serum adiponectin levels are decreased, while proinflammatory cytokines are elevated [18].…”

Section: Abdominal Obesity and Adipokine Imbalancementioning

confidence: 99%

The role of leptin/adiponectin ratio in metabolic syndrome and diabetes

López‐Jaramillo¹,

Gómez-Arbeláez²,

López‐López

et al. 2013

Hormone Molecular Biology and Clinical Investigation

339

299

View full text Add to dashboard Cite

Abstract:The metabolic syndrome comprises a cluster of cardiometabolic risk factors, with insulin resistance and adiposity as its central features. Identifying individuals with metabolic syndrome is important due to its association with an increased risk of coronary heart disease and type 2 diabetes mellitus. Attention has focused on the visceral adipose tissue production of cytokines (adipokines) in metabolic syndrome and type 2 diabetes mellitus, as the levels of the anti-inflammatory adipokine adiponectin are decreased, while proinflammatory cytokines are elevated, creating a proinflammatory state associated with insulin resistance and endothelial dysfunction. In this review, we will give special attention to the role of the leptin/adiponectin ratio. We have previously demonstrated that in individuals with severe coronary artery disease, abdominal obesity was uniquely related to decreased plasma concentrations of adiponectin and increased leptin levels. Leptin/adiponectin imbalance was associated with increased waist circumference and a decreased vascular response to acetylcholine and increased vasoconstriction due to angiotensin II. Leptin and adiponectin have opposite effects on subclinical inflammation and insulin resistance. Leptin upregulates proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6; these are associated with insulin resistance and type 2 diabetes mellitus. In contrast, adiponectin has anti-inflammatory properties and downregulates the expression and release of a number of proinflammatory immune mediators. Therefore, it appears that interactions between angiotensin II and leptin/adiponectin imbalance may be important mediators of the elevated risk of developing type 2 diabetes mellitus and cardiovascular diseases associated with abdominal obesity.

show abstract

Adiponectin expression in human epicardial adipose tissue in vivo is lower in patients with coronary artery disease

Cited by 286 publications

References 24 publications

Increased Epicardial Adipose Tissue Thickness Is Correlated with Ascending Aortic Diameter

Increased Epicardial Adipose Tissue Thickness Is Correlated with Ascending Aortic Diameter

Enhanced Inflammation in Epicardial Fat in Patients With Coronary Artery Disease

The role of leptin/adiponectin ratio in metabolic syndrome and diabetes

Contact Info

Product

Resources

About