Background Adipokines in serum derive mainly from subcutaneous and visceral adipose tissues. Epicardial adipose tissue (EAT), being a relatively small but unique fat depot, probably does not make an important contribution to systemic concentrations of adipokines. However, proximity of EAT to cardiac muscle and coronary arteries allows cells and proteins to penetrate between tissues. It is hypothesized that overexpression of proinflammatory cytokines in EAT plays an important role in pathophysiology of the heart. The aim of the study was to analyze the relationship between echocardiographic heart parameters and adipokines in plasma, epicardial, and subcutaneous fat in patients with obesity and type 2 diabetes mellitus (T2DM). Additionally, we evaluate proinflammatory properties of EAT by comparing that depot with subcutaneous adipose tissue. Methods The study included 55 male individuals diagnosed with coronary artery disease (CAD) who underwent planned coronary artery bypass graft. Plasma concentrations of leptin, adiponectin, resistin, visfatin, apelin, IL-6, and TNF-α, as well as their mRNA and protein expressions in EAT and subcutaneous adipose tissue (SAT) were determined. Results Obesity and diabetes were associated with increased leptin and decreased adiponectin plasma levels, higher protein expression of leptin and IL-6 in SAT, and higher visfatin protein expression in EAT. Impaired left ventricular (LV) diastolic function was associated with increased plasma concentrations of leptin, resistin, IL-6, and adiponectin, as well as with increased expressions of resistin, apelin, and adiponectin in SAT, and leptin in EAT. Conclusions Obesity and T2DM in individuals with CAD have a limited effect on adipokines. Expression of adipokines in EAT and SAT is linked to certain heart parameters, however diastolic dysfunction of the LV is strongly associated with circulating adipokines.

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Edited by Laszlo Nagy Keywords:Cardiac myocyte FAT/CD36 FABPpm PPAR Lipid a b s t r a c t This study reveals that the activation of either PPARa (WY 14 643) or PPARb (GW0742) each induce the translocation of FAT/CD36 from an intracellular pool(s) to the plasma membrane, while PPARb also induces the subcellular redistribution of FABPpm(Got2) to the plasma membrane. In contrast, activation of PPARc failed to induce the subcellular redistribution of FAT/CD36 and FABPpm. These PPARa-, and PPARb-induced changes in the plasmalemmal content of these fatty acid transporters were associated with the concurrent upregulation of fatty acid triacylglycerol esterification (PPARb) and oxidation (PPARa and PPARb). Observed effects of chronic PPAR stimulation were not related to either AMPK or ERK1/2 activation.

Background/Aims: Liver X receptors (LXRα and LXRβ) are ligand-activated transcription factors that regulate expression of genes involved in lipid and cholesterol metabolism. LXR expression has been identified in human and rodent cardiac tissue, however, its role in this tissue remains unclear. The aim of this study was to investigate effects of in vivo LXR activation on lipid metabolism in the rat myocardium under the conditions of low and high lipid intake. Methods: The experiments were performed on male Wistar rats fed for 5 weeks on either low fat diet (LFD) or high fat diet (HFD). Next, the animals were randomly divided into two groups receiving either LXR agonist - T0901317 (10mg/kg/d) or vehicle for the last week of the experiment. After anesthesia samples of the left ventricle and blood were taken. Results: It was found that LXRβ is the dominant isoform in the rat myocardium and the expression of both LXR isoforms did not change after administration of T0901317. Agonist treatment induced hyperlipidemia in low fat fed rats and this effect was amplified in high fat fed rats. LXR agonist elevated content of myocardial triacylglycerols in animals fed on LFD and content of phospholipids in animals fed on HFD. Levels of the remaining examined lipid classes (nonesterified fatty acids, diacylglycerol, free cholesterol, cholesterol esters, ceramide) was decreased or unchaged after LXR activation. Conclusion: We conclude that administration of T0901317 does not lead to severe myocardial lipid accumulation in rats despite of its high plasma availability.

Background/ObjectivesFatty acid handling proteins are involved in the process of accumulation of lipids in different fat tissue depots. Thus, the aim of the study was to estimate the expression of both fatty acid transport and binding proteins in the subcutaneous (SAT) and visceral adipose tissue (VAT) of patients with morbid obesity without metabolic syndrome, as well as the plasma concentrations of these transporters.Subjects/MethodsProtein (Western blotting) and mRNA (Real-time PCR) expression of selected fatty acid handling proteins was assessed in the visceral and subcutaneous adipose tissue of 30 patients with morbid obesity. The control group consisted of 10 lean age-matched patients. Plasma levels of fatty acid protein transporters were also evaluated using ELISA method. Moreover, total plasma fatty acid composition and concentration was determined by gas-liquid chromatography (GLC).ResultsSignificant increase in fatty acid translocase (FAT/CD36) mRNA (P = 0.03) and plasmalemmal (P = 0.01) expression was observed in VAT of patients with morbid obesity vs. lean subjects together with elevation of lipoprotein lipase (LPL), as well as peroxisome proliferator-activated receptor γ (PPARγ) in both examined compartments of adipose tissue. Moreover, in obese subjects plasma concentration of RBP4 was markedly elevated (P = 0.04) and sCD36 level presented a tendency for an increase (P = 0.08) with concomitant lack of changes in FABP4 concentration (P > 0.05).ConclusionsFatty acid transport into adipocytes may be, at least in part, related to the increased expression of FAT/CD36 in the VAT of morbidly obese patients, which is accompanied by augmented expression of LPL, as well as PPARγ. Probably, alternations in plasma concentrations of RBP4 and sCD36 in obese patients are associated with “unhealthy” fat distribution.