Epicardial Adipose Tissue: New Kid on the Block

Over the last 2 decades, understanding of epicardial adipose tissue (EAT) significantly changed from an innocent bystander, protecting the coronary arteries from physical damage, to an inflammatory active endocrine organ that may influence development of atherosclerosis in the coronary arteries. EAT is a visceral adipose tissue, surrounding the heart and the coronary arteries. It is associated with cardiovascular risk factors and with coronary artery plaque burden. In addition, increasing evidence identifies a link of EAT with prevalent and incident coronary heart disease in patient cohorts as well as general population-based studies. This review article will give an overview over the existing literature on this emerging topic with special focus on the implications of EAT as a potential novel marker of cardiovascular risk burden.     

Different Expression and Function of the Endocannabinoid System in Human Epicardial Adipose Tissue in Relation to Heart Disease

Background

The endocannabinoid system reportedly plays a role in the pathogenesis of cardiovascular diseases. This system is expressed also in adipose tissue, which could thus be involved in cardiac disorders through modulation of metabolically triggered inflammation. The current study aims to determine the relevance of the endocannabinoid system in epicardial adipose tissue in heart disease.

Methods

Expression of the endocannabinoid receptors CB1 and CB2, and of the endocannabinoid-degrading enzyme, fatty acid amidohydrolase, and activation of protein kinase A (PKA), phospholipase C (PLC), protein kinase C (PKC), endothelial nitric oxide synthase (eNOS) and inducible (i)NOS, and extracellular signal-regulated kinases 1 and 2 (ERK1/2) (a member of the reperfusion-injury salvage kinase pathway), were analyzed by Western blot in patients after coronary artery bypass surgery (ischemics; N = 18) or valve surgery (nonischemics; N = 15) and in preadipocytes isolated from epicardial adipose tissue.

Results

In ischemics, the CB1-to-CB2 expression ratio shifted toward CB1 and was accompanied by higher PKA activation. In contrast, in nonischemics, CB2, fatty acid amidohydrolase, PLC and PKC, and ERK1/2 were upregulated. Moreover, NO production and iNOS-to-eNOS ratios were higher in preadipocytes from ischemics.

Conclusions

These results show a different modulation and functioning of the endocannabinoid system in ischemics compared with nonischemics. Hence, while CB2, PLC and PKC, ERK1/2, and eNOS are more strongly expressed in patients without ischemic heart disease, high CB1 and PKA expression is associated with low survival intracellular pathway activation and high iNOS activation in ischemic heart disease patients. The changes in the endocannabinoid system in ischemics may contribute to cardiac dysfunction and therefore represents a potential therapeutic target.     

Echocardiographic Determination of Epicardial Adipose Tissue in Healthy Bonnet Macaques

Background: Nonhuman primates have served as models for human cardiovascular (CV) and metabolic diseases. Recently, echocardiographic measurement of epicardial adipose tissue (EAT) thickness has been shown to be a reliable marker of visceral adiposity, and greater EAT is associated with increased CV risk, left ventricular (LV) hypertrophy, and metabolic syndrome. The objective of the present study was to determine EAT thickness in apparently healthy bonnet macaques and assess its relations with anthropometric and CV variables. Methods: Echocardiography was performed on 61 monkeys (41 females and 20 males, mean age 13.0 ± 4.7 years). EAT was measured on the right ventricular free wall in parasternal windows. Applanation tonometry was performed in 25 unselected monkeys using a SphygmoCor pulse wave system. Results: The mean EAT thickness was 2.4 ± 0.6 mm. EAT thickness was directly correlated with age (r = 0.26, P = 0.04), male gender (r = 0.47, P < 0.01), weight (r = 0.42, P < 0.01), crown–rump length (r = 0.45, P < 0.01), BMI (r = 0.38, P < 0.01), diastolic BP (r = 0.46, P = 0.01), and HR (r =−0.49, P < 0.01). EAT thickness also correlated with augmentation index (r = 0.42, P = 0.04), LV mass (r = 0.48, P < 0.01), and left atrial (LA) diameter (r = 0.26, P = 0.04). Intra‐ and interobserver coefficients of variation between measurements of EAT were 1.4% and 3.7%. On multivariate analysis adjusting for age, gender, weight, and CRL, EAT was independently related to age and weight (r²= 0.47, P < 0.01). Conclusion: This study found echocardiography to be a feasible and practical method to evaluate EAT in nonhuman primates. In bonnet macaques, EAT thickness correlates with LV and LA dimensions and augmentation index, and is independently related to age and weight. (ECHOCARDIOGRAPHY 2010;27:180‐185)     

High Visceral Adipose Tissue to Subcutaneous Adipose Tissue Ratio as a Predictor of Mortality in Acute Respiratory Distress Syndrome

Background

We aimed to further determine the relationship between the areas of visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and the ratio of VAT to SAT (VAT/SAT) with the outcomes of acute respiratory distress syndrome (ARDS) patients.

超重和肥胖成人心外膜脂肪组织和胰岛素抵抗的关系研究

目的研究超重和肥胖成人胰岛素敏感性、胰岛素抵抗及心外膜脂肪组织和胰岛素抵抗的关系。方法收集2005年3月至2005年12月在我院体检中心符合入选标准的资料210份,均具人体指标测量、空腹血生化检查和经超声测量心外膜脂肪组织厚度、腹壁脂肪厚度(SFT)等数据,根据中国肥胖工作组推荐的判定标准,分为超重肥胖组和体重正常组。采用稳态模式胰岛素抵抗指数(HOMA-IR)评价胰岛素抵抗。用SPSS 13.0软件进行统计分析。结果超重肥胖组SI显著低于体重正常组(P<0.01),FINS、HOMA-IR显著高于体重正常组(P<0.01),心外膜脂肪组织厚度明显厚于体重正常组(P<0.01);控制年龄、性别、腰围影响因素进行偏相关分析,显示心外膜脂肪组织厚度和FINS、HOMA-IR成正相关,相关系数分别为0.239、0.249,P<0.05;和SI成负相关,相关系数为0.249,P<0.05,SFT则与各个因素无相关性;逐步法多元线性回归分析显示,心外膜脂肪组织厚度和HOMA-IR呈正相关,标准化偏回归系数0.309,P<0.01,而SFT仅和BMI呈正相关。结论超重肥胖成人存在胰岛素敏感性降低、胰岛素抵抗,心外膜脂肪组织厚度和胰岛素抵抗成正相关,可能是新的心血管和代谢疾病的危险因素。     

2型糖尿病合并代谢综合征患者心外膜脂肪特点

目的探讨2型糖尿病合并代谢综合征患者心外膜脂肪特点。方法选择2型糖尿病患者120人为研究对象,测量身高、体重、腰围、臀围和血压,抽空腹血测量血糖、糖化血红蛋白、甘油三酯和高密度脂蛋白胆固醇,利用双能X线测量身体脂肪和肌肉,超声心动图测量心外膜脂肪。Logistic多元回归分析用于评价心外膜脂肪和各变量的联系程度。结果合并代谢综合征的糖尿病患者腰围、腰臀比、甘油三酯、全身脂肪、男性型脂肪、心外膜脂肪、高血压和冠心病患病率均高于未合并代谢综合征者,腰围、甘油三酯和男性型脂肪是心外膜脂肪增加的独立危险因素,而高密度脂蛋白胆固醇属于独立保护因素。结论 2型糖尿病合并代谢综合征者的心外膜脂肪较未合并代谢综合征者增多,且其厚度与腰围、甘油三酯、男性型脂肪和高密度脂蛋白胆固醇密切相关。     

Increased Epicardial Adipose Tissue is Associated with the Extent of Aortic Dissection

BackgroundEpicardial adipose tissue (EAT) is a biologically active organ that has endocrine and paracrine functions. Endothelial dysfunction, systemic, and local inflammatory response, due to bio-active molecules produced by EAT, may affect aortic dissection propagation and extent. We investigated the association between EAT thickness and the extent of aortic dissection.MethodsWe retrospectively enrolled 78 patients with aortic dissection diagnosed by thoracoabdominal Computerized Tomography (CT). EAT was measured from the thickest part of the perpendicular plane between the pericardium and free wall of the right ventricle using CT. Aortic dissection length was measured from the beginning to the end of the dissection flap at sagittal images.ResultsWe included 78 patients with the mean age of 63.9 ± 11.7 and 57 (73.5%) patients were male. Dissection length was correlated positively with EAT (r = 0.409, p < 0.001), body mass index (r = 0.408, p = 0.018), and admission systolic blood pressure (r = 0.830, p = 0.026) whereas an inverse correlation existed between age and dissection length (r = −0.318, p = 0.005). Multivariate analysis identified age and EAT as independent predictors of dissection length.ConclusionIncreased EAT was independently associated with the extent of aortic dissection. We think that either paracrine and endocrine functions of EAT might have contributed to the extent of aortic dissection.     

棕色脂肪组织特异性基因在抵抗肥胖中作用的研究

目的通过研究高脂饮食诱导肥胖与肥胖抵抗大鼠肩胛间棕色脂肪组织中UCP-1、PGC-1α、Dio-2的表达情况以及电针刺激对肥胖大鼠UCP-1、PGC-1α表达的影响,探讨棕色脂肪组织特异性基因在抵抗肥胖中的作用。方法 40只雄性SD大鼠,按体重随机分为高脂实验组(n=28)和基础对照组(n=12)。分别给予高脂饲料和基础饲料喂养。高脂饮食5周末,将高脂实验组大鼠体重大于基础对照组最大体重者归为饮食诱导肥胖大鼠(DIO),将高脂实验组大鼠体重低于对照组平均体重者归为饮食诱导肥胖抵抗大鼠(DIO-R)。从DIO随机取6只为肥胖组(n=6)与肥胖抵抗组(n=6)、基础对照组(n=6),比较各组大鼠体重、两种脂肪重水平,使用实时荧光定量PCR及Western blot方法比较三组肩胛间棕色脂肪组织中UCP-1、PGC-1α、Dio-2表达水平的差异。在DIO大鼠中再取10只随机分为:肥胖组(Ob组,n=5)、电针刺激组(EA组,n=5)与基础对照组(n=5)以基础饲料适应性喂养1周后,其中EA组选取足三里、三阴交给予电针刺激,每周3次,每次30 min,观察摄食量及体重变化。6周后使用实时荧光定量PCR及Westernblot方法比较3组大鼠棕色脂肪组织中UCP-1、PGC-1α表达水平的差异。结果 DIO组明显高于DIO-R组,DIO-R组大鼠肩胛间棕色脂肪组织重及Dio-2、PGC-1α、UCP-1mRNA表达水平明显高于DIO大鼠(P<0.05)。高脂组大鼠PGC-1α、Dio-2m RNA表达水平均低于对照组大鼠(P<0.05);DIO-R组大鼠UCP-1 mRNA表达水平高于对照组大鼠(P<0.05)。DIO大鼠UCP-1蛋白水平表达低于基础对照组及DIO-R大鼠(P<0.05)。电针刺激6周后,电针刺激组大鼠棕色脂肪组织中UCP-1、PGC-1αmRNA及蛋白水平表达均高于Ob组及对照组(P<0.05)。电针刺激组大鼠体重、摄食量低于肥胖组大鼠(P<0.05)。结论高脂饮食条件下,SD大鼠表现为明显的肥胖易感性差异。饮食诱导肥胖抵抗大鼠棕色脂肪组织重及特异性基因表达升高。电针刺激增加了棕色脂肪组织特异性基因表达,减少摄食量。棕色脂肪组织特异性基因表达在抵抗肥胖中有重要作用。