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The data are presented as the median values and the 25th and 75th quartiles. The clinical and demographic data of the study patients are shown in Table 2. Patients were divided into 2 groups, based on whether they had VO present; the first group included 54 patients with VO, the second group included 30 people without VO Table 3. Patients were comparable in age, the presence of risk factors for CVD i.

A similar pattern was observed in the visualization of the intrauterine tract of the abdominal aorta, such that the volume of the fat deposits in patients with VO was 1. However, for the thoracic compartment, there was no difference in the volume of paraaortic AT between the 2 patient groups. Whereas in patients without VO, the prevalence of fatty deposits around the right coronary artery and the lower third of the envelope artery was 6. The volume of fat deposits of the paracoronary arteries did not depend on the magnitude of the VAT or the volume of the PVAT of the aorta.

In addition, patients with VO were characterized by hyperinsulinemia, an increase in the concentration of C-peptides, compared to patients without VO. The presence of atherogenic dyslipidemia and IR was accompanied by the formation of widespread atherosclerotic vascular lesions in patients with CAD and VO. Based on the results of angiographic examinations and the duplex scanning of blood vessels, isolated CAD was recorded in In addition, 3 or more lesions of the coronary vessels predominated, which occurred in As a result of the evaluation of the adipokine balance parameters in the blood serum of patients with CAD Table 6 , it was found that for patients with VO, the level of leptin was 1.

Leptin resistance was confirmed by FLI, which was 2. On the contrary, the concentration of adiponectin in the serum of patients with VO was Additionally, the level of anti-inflammatory IL was 2. The correlation analysis confirmed the relationship between EAT thickness and the serum concentrations of adipokines. In patients without VO, such connections were not established. Over the course of the analysis, there was no evidence of a correlation between VAT magnitude and the thickness PVAT of the coronary artery.

According to the literature, EAT is a type of visceral AT localized near the myocardium and around the coronary arteries [ 21 ]. VAT and EAT have the same embryological origin, and the increase in the size of either fat store is associated with calcification of the coronary arteries [ 22 , 23 ], as well as the development of CAD [ 24 ].

Some researchers believe that an increase in the thickness of epicardial fat reflects the presence of visceral obesity in the body and serves as a prognostic marker of coronary heart disease and its associated complications [ 25 ]. The results obtained in this study show that EAT thickness is directly dependent on the value of the VAT; this concurs with the results of previous studies [ 26 , 27 ].

Our findings also show that the presence of a direct connection between an increase in EAT thickness and LV hypertrophy, as well as insulin resistance. Similar properties are also present with VAT [ 22 , 28 ]. Despite the presence of this bond, epicardial adipocytes have unique properties that distinguish them from the fat cells of other depots [ 28 ]. The cells of white and brown AT differ significantly from each other. The cells of white AT have one large fatty vial inside that occupies almost the entire cell and pushes its core to the periphery, which becomes flattened.

In brown AT adipocytes, there are several small fat drops and many mitochondria that contain iron in cytochromes , which is responsible for the brown color of the tissue. Under physiological conditions, adipocytes of EAT perform a number of important functions for the myocardium: metabolic absorb excess FFA and act as a source of energy under ischemic conditions , thermogenic protect the myocardium from overheating , and mechanical, as well as the synthesis of adiponectin and adrenomedullin-possessing cardioprotective properties [ 24 , 29 ].

However, against the background of obesity and the progression of coronary atherosclerosis, the phenotype of EAT adipocytes from brown to white changes due to activation of the IL-6 signaling pathway of JAK-STAT3 [ 30 ]. In addition, for patients with coronary artery disease and VO, against hypertension, hyperleptinemia, leptin resistance, and a reduction in adiponectin concentration were recorded.

However, the metabolic processes accompanying hypertrophy and changes in the phenotypes of EAT adipocytes differ from those in visceral adipocytes. Therefore, we have demonstrated that an increase in VAT is associated with leptin hypoproducts against adiposopathy, as well as with the development of leptin resistance. Meanwhile, the EAT thickness was inversely related to the concentration of leptin and the FLI index one of the main leptin-resistance markers.

Perivascular fat is located around vessels of different sizes and does not have barriers separating it from the adventitia of the vessel [ 32 ]; therefore, this results in synthesized cytokines and chemokines acting directly on the vascular wall, potentiating vasospasm, endothelial dysfunction, proliferation of smooth muscle cells, migration of leukocytes in the intima, and fibrosis [ 33 ].

A large amount of data supports regional, phenotypic, and functional differences between deposits of different localizations [ 34 ]. The results obtained in this report confirm this assumption. We did not find a correlation between PVAT thickness and the thickness of the coronary arteries; while for EAT thickness, this relationship was recorded and was of a direct consequence. Interestingly, the PVAT of the coronary artery is slightly anomalous, because it resembles the phenotype of white AT, but includes adipocytes of different sizes and differentiated statuses, similar to brown AT [ 35 , 36 ].

EAT and PVAT coronary arteries have different phenotypes, but the presence of a common microcirculation network and direct anatomical proximity allows these tissues to interact and influence each other. Therefore, the thickness of the perivascular deposits of the left coronary artery depended only on EAT thickness right ventricle, which it directly contacts with , and the vessels of the right side of the heart from the EAT left ventricle. Evaluation of the volume of para-aortal AT showed no difference in the thoracic region, depending on the presence of VO.

The heterogeneity of the PVAT of a vessel can be important for the realization of its protective or pro-atherogenic function. In the course of our study, it was shown that the metabolic potential of PVAT of the abdominal aorta is similar to VAT, as evidenced by the correlations with the concentration of FFA, leptin, and FLI, while such connections were not discovered in the thoracic region. Previously, such connections were demonstrated only in subcutaneous AT, whereas for other visceral deposits such connections are not characteristic.

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The results indicate the potential of the depot data as a drug application point. The study of the molecular basis of PVAT and EAT function can provide a more complete understanding of the etiopathogenetic mechanisms of CVD and develop an effective strategy for their prevention and control. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Abstract The aim of this study was to determine the relationship between the thickness of epicardial adipose tissue EAT and perivascular adipose tissue PVAT and the adipokine-cytokine profile of patients with coronary heart disease, which can be of significant importance for predicting the course of cardiovascular disease CVD.

Introduction Obesity is a rapidly growing problem that is becoming an epidemic on a global scale, affecting both children and adults [ 1 , 2 ]. Study subjects Eighty-four patients with CAD, comprising 65 men and 19 women, whose mean age was Download: PPT. Table 1. Fig 1. Quantitative assessment of the thickness of epicardial adipose tissue along the anterior wall of the right ventricle, as well as the thickness of the epicardial adipose tissue orange contour along the posterior wall of the left ventricle.

Fig 3. Quantitative assessment of paracoronary fat tissue at the level of the proximal segment of the anterior descending artery, the middle third of the anterior descending artery, and the proximal segment of the right coronary artery. ADI levels were found to be highest in cardioembolic stroke patients and lowest in intracranial atherothrombotic stroke groups [ 30 , 54 ].

Chen and colleagues showed plasma adiponectin to be significantly lower in ischemic stroke patients than in healthy subjects. According to the authors ADI level remains an independent stroke risk factor [ 57 ]. They did not find differences of plasma ADI levels between patients with small- and large-artery infarction [ 57 ].

Similarly both extracranial atherothrombotic stroke and small-artery stroke patients have displayed the same levels of plasma ADI [ 54 ]. Both these results are partly in contrast with our finding. Our stroke patients showed evidently lower levels of ADI than controls, and the lowest levels were found in men with atherothrombotic stroke and in women with small-artery stroke [ 30 ].

However, several studies found no relationship of ADI levels and IS incidence in both older women [ 58 ] and men [ 14 ]. Rajpathak and colleagues also found circulating levels of ADI not to be independently associated with an increased risk of IS in postmenopausal women. In these patients ADI levels were dependent on obesity and other cardiovascular disease risk factors [ 59 ]. Adiponectin levels were significantly higher among the stroke participants with coronary heart disease compared to those without it.

Confusion in the literature partly relates to complexities in interpreting benefits of higher levels of adiponectin versus its pathological increase as in heart failure [ 60 ].

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An alternative explanation sees adiponectin overproduced in response to vascular inflammation to counter the atherosclerotic process in arteries [ 48 , 60 ]. Hypoadiponectinemia can serve as an independent predictor of mortality after IS. Efstathiou et al. Plasma ADI levels were found to be positively associated with age, despite higher frequency of vascular risk factors in older patients [ 61 , 62 ]. It has been suggested that aging and advanced stages of cardio- and cerebrovascular diseases may trigger a counterregulatory response that raises plasma ADI [ 60 ]. Atrial fibrillation is burdened by enhanced systemic inflammation and platelet activation.

In the study it was documented by increased blood levels of soluble proinflammatory marker, a CDreceptor ligand CD40L , and low levels of ADI even after administration of anticoagulants [ 63 ]. Low levels of ADI in patients with atrial fibrillation suggested a role of ADI to favor platelet activation in vivo [ 63 ].

According to other reports, lower baseline ADI concentrations inversely correlated with poor outcomes of IS independently of other adverse predictors [ 50 ]. All differences between stroke subgroups, stratified according to adiponectin levels, did not reach significance, suggesting relatively weak association of ADI with the etiology of IS [ 50 , 58 ]. It has been demonstrated experimentally that the decreased secretion of ADI in obesity alters lipid metabolism and insulin sensitivity in the liver.

However, administration of recombinant adiponectin to adiponectin-deficient obese mice fed a high-fat diet dramatically alleviated hepatomegaly, steatosis, and inflammation [ 64 ]. Exogenous administration of ADI might counteract the consequences of obesity state and activate its antiatherogenic, vasoprotective, and anticancer actions [ 65 ].

Direct supplementation of recombinant ADI in human subjects would be extremely expensive. An alternative approach is to use pharmacological or dietary intervention to enhance ADI actions in target tissues. Thiazolidinediones rosiglitazone, pioglitazone , inhibitors of angiotensin-converted enzyme, and angiotensin II blockers reinforce positive vascular effects [ 49 , 50 ]. Statins, thought to improve vascular endothelial functions, have shown ambiguous role when atorvastatin was not proved to decrease ADI levels in diabetic or prediabetic patients [ 66 ].

Metformin, a commonly used antidiabetic drug, was shown to mimic the action of ADI and may be potentially used in supplementation of ADI [ 49 ]. Other possible treatment targets might be proinflammatory cytokines and chemokines or their receptors, through the use of their agonists or monoclonal antibodies [ 65 ].

The name resistin RES of this adipokine has been derived from the observation that it induced insulin resistance in mice. Furthermore, in this study of neurologically intact individuals, CSF resistin levels did not correlate with age or HOMA-IR index, and they remained unaltered by diabetic status [ 67 ].

This might be explained by the fact that RES emerges dominantly as a critical mediator of insulin resistance associated with inflammatory settings or sepsis [ 18 ]. According to other authors RES could induce similar effects to those of leptin. Increased levels of RES seem to be positively associated with atherosclerosis due to induction of endothelial cells and consequent expression of adhesion molecules, chemokines, and cell proliferation [ 65 , 68 ].

Resistin can increase the risk of stroke by promoting systemic inflammation and endothelial dysfunction, both playing a significant role in atherosclerosis [ 68 ]. Rajpathak et al. The effects of resistin on stroke risk could not be explained by the obesity-associated pathways and might involve additional unidentified biological mechanisms [ 59 ].

Resistin is supposed to mediate intensity of ischemic cerebrovascular events. The participation of RES in endothelial dysfunction in insulin-resistant patients related to its direct effect on endothelial cells promoting the release of endothelin-1 [ 70 ]. The proliferative effect of RES was suggested to underlie the increased incidence of restenosis after artery stenting common among diabetic patients [ 70 ]. Apelin APE is a bioactive peptide that was originally identified as the endogenous ligand of the orphan G-protein-coupled receptor.

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In obesity, increased levels in plasma and adipose tissue were reported [ 65 ]. APE was associated with a positive hemodynamic profile, having a positive inotropic effect in normal and failing rat hearts [ 65 ]. Reduced apelin levels were found in patients affected by single atrial fibrillation and chronic heart failure [ 72 , 73 ]. Apelin has been recently identified as an angiotensin II homologue with an impact on vasoreactivity [ 74 ]. In contrast, APE treatment was reported to have beneficial effect on aortic wall, causing its relaxation [ 74 ]. The function of APE in development of cerebrovascular disorders is not fully clear.

A recently reported case-control study did not find any differences in apelin plasma levels between IS patients and healthy controls [ 75 ]. In humans apelin levels in acute IS were not elevated, contrary to leptin levels [ 75 ]. Visfatin VIS is a recently discovered adipokine, secreted mainly by visceral adipose tissue [ 71 ]. According to other authors, VIS plasma levels were shown to correlate with measures of global obesity but not visceral-fat mass or waist-to-hip ratio [ 18 ]. VIS is an insulin-mimetic adipokine that was originally discovered in liver, skeletal muscle, and bone marrow as a growth factor for B lymphocyte precursors.

It was upregulated in models of acute lung injury and sepsis.

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Circulating visfatin levels closely correlated with white adipose tissue accumulation. Relationship of VIS and type 2 diabetes was also described [ 18 ]. Role of VIS in stroke has been studied and reported by several authors. After adjustment for diabetes, hypertension, dyslipidemia, and age, visfatin was assessed as independent predictor of acute IS [ 75 ]. Predictive role of VIS was demonstrated in 6-month follow-up [ 76 ]. VIS seems to be a prognostic factor of cardiovascular mortality [ 75 ]. Visfatin seems to have a key role in plaque destabilization, associated with its increased expression in macrophages of human unstable carotic and coronary atherosclerosis.

In microarray VIS gene was markedly enhanced in carotic plaques in symptomatic individuals compared with plaques in asymptomatic individuals [ 77 ]. The relationship between inflammatory markers and VIS levels in patients with symptomatic carotic atherosclerosis supported an inflammatory role of VIS as a mediator in carotic atherosclerosis [ 77 ] and future stroke. Increase in rates of overweight and obese people in industrial countries has awakened the interest in the role of adipose tissue in metabolic and hormonal balance in the human body.

Adipokines, hormones released by adipose tissue, are divided into two groups. One includes those with anti-inflammatory, antidiabetic, and anabolic functions such as adiponectin.


The other includes hormones with proinflammatory, prodiabetic, and catabolic functions, for example, leptin, resistin, visfatin, and probably apelin. Now we know that adipokines regulate metabolism via hypothalamic receptors, and they also function as cytokines, being linked to innate immunity. Moreover, adipokines that appear to regulate endovascular compartment can be crucial for later development of arterial stiffness. Increase in adipose tissue disturbs the balance in adipokine production and activity.

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Participation of certain adipokines in pathomechanisms of ischemic stroke has been proved by independent studies. However, studies have shown them to be both obesity-dependent and obesity-independent factors. It is obvious that there are differences between populations in prevalence of obesity, as well as in diet, calorie intake, and level of physical activity.

Interindividual variability of impact of adipokines on target tissues of subjects in high risk of IS poses the question about the role of genetic background of adipocytes' reactivity to environmental influence. Precise mechanism of functioning of adipokines is probably dependent on other not fully known factors. Despite the volume of current information about adipokines, our knowledge is still incomplete and requires further studies.

Even so, it is possible to link excessive cumulation of adipose tissue to ischemic stroke risk. The authors declare that there is no conflict of interests regarding publication of this paper. Europe PMC requires Javascript to function effectively. Recent Activity. The snippet could not be located in the article text.

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This may be because the snippet appears in a figure legend, contains special characters or spans different sections of the article. Int J Endocrinol. Published online Dec PMID: This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC.

Abstract Cerebrovascular disorders, particularly ischemic stroke, are one of the most common neurological disorders. Introduction Adipose tissue is a highly specialized organ that stores excess energy and releases it when needed by other tissues [ 1 ]. Ischemic Stroke and Obesity Stroke, a leading course of death or disability, shares many risk factors with cardiovascular diseases CVD , such as age, smoking, hypertension, diabetes mellitus, inactivity, overweight or obesity, and dyslipidemia [ 1 ].

Adipokines and Ischemic Stroke 3. Leptin Leptin LEP is expressed mostly in adipose tissue, although low levels were found in other organs [ 19 ]. Adiponectin Adiponectin ADI is one of the most abundant adipokines produced by adipocytes. Resistin The name resistin RES of this adipokine has been derived from the observation that it induced insulin resistance in mice.

Apelin Apelin APE is a bioactive peptide that was originally identified as the endogenous ligand of the orphan G-protein-coupled receptor. Visfatin Visfatin VIS is a recently discovered adipokine, secreted mainly by visceral adipose tissue [ 71 ]. Conclusion Increase in rates of overweight and obese people in industrial countries has awakened the interest in the role of adipose tissue in metabolic and hormonal balance in the human body.

Conflict of Interests The authors declare that there is no conflict of interests regarding publication of this paper. References 1. Levine T. Adipose tissue and overweight. In: Pioli S. Metabolic Syndrome and Cardiovascular Disease. Tarantal A. Obesity and lifespan health—importance of the fetal environment. Trayhurn P. Physiological role of adipose tissue: white adipose tissue as an endocrine and secretory organ. Proceedings of the Nutrition Society. Vasoactive factors and inflammatory mediators produced in adipose tissue.

In: Fantuzi G. Matarese G. Leptin in autoimmune diseases. In: Fantuzzi G. Rocha B.

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Circulating levels of adipokines in Parkinson's disease. Journal of the Neurological Sciences. Gustafson D. Adiposity hormones and dementia. Boden-Albala B. Metabolic syndrome and ischemic stroke risk. Northern Manhattan Study. The association of obesity and cerebrovascular disease in young adults—a pilot study. Acta Clinica Croatica. Milionis H. Components of the metabolic syndrome and risk for first-ever acute ischemic nonembolic stroke in elderly subjects. Suk S. Abdominal obesity and risk of ischemic stroke: the Northern Manhattan Stroke Study.

Winter Y. Contribution of obesity and abdominal fat mass to risk of stroke and transient ischemic attacks. Kurth T. Body mass index and the risk of stroke in men. Book Description Humana Press Inc. Condition: New. Language: English. Brand new Book. Seller Inventory LIE More information about this seller Contact this seller. Seller Inventory AAV Book Description Humana Press, New Book. Delivered from our UK warehouse in 4 to 14 business days. Established seller since Seller Inventory LQ Shipped from UKs. Book Description Humana Pr Inc,