scholarly journals Perivascular Adipose Tissue and Cardiometabolic Disease

2013 ◽  
Vol 5 (1) ◽  
pp. 13
Author(s):  
Anna Meiliana ◽  
Andi Wijaya
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Blood Vessels ◽  
Vascular Function ◽  
Immune Cell ◽  
The Body ◽  
Cardiometabolic Disease ◽  
Perivascular Adipose Tissue ◽  
Nitric Oxide Signaling ◽  
Fat Depots

BACKGROUND: Obesity is associated with insulin resistance, hypertension, and cardiovascular disease, but the mechanisms underlying these associations are incompletely understood. Microvascular dysfunction may play an important role in the pathogenesis of both insulin resistance and hypertension in obesity.CONTENT: Perivascular adipose tissue (PVAT) is a local deposit of adipose tissue surrounding the vasculature. PVAT is present throughout the body and has been shown to have a local effect on blood vessels. The influence of PVAT on the vasculature changes with increasing adiposity. PVAT similarly to other fat depots, is metabolically active, secreting a wide array of bioactive substances, termed ‘adipokines’. Adipokines include cytokines, chemokines and hormones that can act in a paracrine, autocrine or endocrine fashion. Many of the proinflammatory adipokines upregulated in obesity are known to influence vascular function, including endothelial function, oxidative stress, vascular stiffness and smooth muscle migration. Adipokines also stimulate immune cell migration into the vascular wall, potentially contributing to the inflammation found in atherosclerosis. Finally, adipokines modulate the effect of insulin on the vasculature, thereby decreasing insulin-mediated muscle glucose uptake. This leads to alterations in nitric oxide signaling, insulin resistance and potentially atherogenesis.SUMMARY: PVAT surrounds blood vessels. PVAT and the adventitial layer of blood vessels are in direct contact with each other. Healthy PVAT secretes adipokines and regulates vascular function. Obesity is associated with changes in adipokine secretion and the resultant inflammation of PVAT. The dysregulation of adipokines changes the effect of PVAT on the vasculature. Changes in perivascular adipokines secretion in obesity appear to contribute to the development of obesity-mediated vascular disease.KEYWORDS: obesity, perivascular adipose tissue, PVAT, cardiometabolic disease, adipokine

Crosstalk between adipose tissue and blood vessels in cardiometabolic syndrome: implication of steroid hormone receptors (MR/GR)

2014 ◽  
Vol 19 (2) ◽  
Author(s):  
Sarah Elisabeth Louise Even ◽  
Maria Gabriela Dulak-Lis ◽  
Rhian M. Touyz ◽  
Aurelie Nguyen Dinh Cat
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Blood Vessels ◽  
Vascular Function ◽  
Hormone Receptors ◽  
Steroid Hormone Receptors ◽  
Perivascular Adipose Tissue ◽  
Cardiometabolic Syndrome ◽  
Cardiovascular Abnormalities ◽  
Obesity And Diabetes

AbstractCrosstalk between adipose tissue and blood vessels is vital to vascular homeostasis and is disturbed in cardiovascular and metabolic diseases such as hypertension, diabetes and obesity. Cardiometabolic syndrome (CMS) refers to the clustering of obesity-related metabolic disorders such as insulin resistance, glucose and lipid profile alterations, hypertension and cardiovascular diseases. Mechanisms underlying these associations remain unclear. Adipose tissue associated with the vasculature [known as perivascular adipose tissue (PVAT)] has been shown to produce myriads of adipose tissue-derived substances called adipokines, including hormones, cytokines and reactive oxygen species (ROS), which actively participate in the regulation of vascular function and local inflammation by endocrine and/or paracrine mechanisms. As a result, the signaling from PVAT to the vasculature is emerging as a potential therapeutic target for obesity and diabetes-related vascular dysfunction. Accumulating evidence supports a shift in our understanding of the crucial role of elevated plasma levels of aldosterone in obesity, promoting insulin resistance and hypertension. In obesity, aldosterone/mineralocorticoid receptor (MR) signaling induces an abnormal secretion of adipokines, ROS production and systemic inflammation, which in turn contribute to impaired insulin signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular abnormalities. Thus, aldosterone excess exerts detrimental metabolic and vascular effects that participate to the development of the CMS and its associated cardiovascular abnormalities. In this review, we focus on the physiopathological roles of corticosteroid receptors in the interplay between PVAT and the vasculature, which underlies their potential as key regulators of vascular function.

scholarly journals Similarity of mouse perivascular and brown adipose tissues and their resistance to diet-induced inflammation

2011 ◽  
Vol 301 (4) ◽  
pp. H1425-H1437 ◽  
Author(s):  
Timothy P. Fitzgibbons ◽  
Sophia Kogan ◽  
Myriam Aouadi ◽  
Greg M. Hendricks ◽  
Juerg Straubhaar ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Vascular Function ◽  
Immune Cell ◽  
Expression Profiles ◽  
Immunohistochemical Analysis ◽  
Macrophage Infiltration ◽  
Interscapular Brown Adipose Tissue ◽  
Perivascular Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Brown Adipose

Thoracic perivascular adipose tissue (PVAT) is a unique adipose depot that likely influences vascular function and susceptibility to pathogenesis in obesity and the metabolic syndrome. Surprisingly, PVAT has been reported to share characteristics of both brown and white adipose, but a detailed direct comparison to interscapular brown adipose tissue (BAT) has not been performed. Here we show by full genome DNA microarray analysis that global gene expression profiles of PVAT are virtually identical to BAT, with equally high expression of Ucp-1, Cidea, and other genes known to be uniquely or very highly expressed in BAT. PVAT and BAT also displayed nearly identical phenotypes upon immunohistochemical analysis, and electron microscopy confirmed that PVAT contained multilocular lipid droplets and abundant mitochondria. Compared with white adipose tissue (WAT), PVAT and BAT from C57BL6/J mice fed a high-fat diet for 13 wk had markedly lower expression of immune cell-enriched mRNAs, suggesting resistance to obesity-induced inflammation. Indeed, staining of BAT and PVAT for macrophage markers (F4/80 and CD68) in obese mice showed virtually no macrophage infiltration, and FACS analysis of BAT confirmed the presence of very few CD11b+/CD11c+ macrophages in BAT (1.0%) compared with WAT (31%). In summary, murine PVAT from the thoracic aorta is virtually identical to interscapular BAT, is resistant to diet-induced macrophage infiltration, and thus may play an important role in protecting the vascular bed from inflammatory stress.

scholarly journals Immune spleen cells attenuate the inflammatory profile of the mesenteric perivascular adipose tissue in obese mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Renée de Nazaré Oliveira da Silva ◽  
Rosangela Aparecida Santos-Eichler ◽  
Carolina Dias ◽  
Stephen Fernandes Rodrigues ◽  
Dominik S. Skiba ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Immune Cell ◽  
Protective Role ◽  
Standard Diet ◽  
Spleen Cells ◽  
Perivascular Adipose Tissue ◽  
Fat Depots ◽  
Cytokine Levels ◽  
Hematoxylin And Eosin ◽  
Inflammatory Profile

AbstractThe perivascular adipose tissue (PVAT) differs from other fat depots and exerts a paracrine action on the vasculature. The spleen has an important role in the immune response, and it was observed to have either a protective role or a contribution to obesity-related diseases. However, the relation between spleen and PVAT is elusive in obesity. We investigated the role of spleen in the inflammatory profile of the mesenteric PVAT (mPVAT) from mice fed a high-fat diet (HFD) for 16 weeks. Male C57Bl/6 mice were sham-operated or splenectomized (SPX) and fed a HFD for 16 weeks. mPVAT morphology was evaluated by hematoxylin and eosin staining, infiltrated immune cells were evaluated by flow cytometry, inflammatory cytokines were evaluated by ELISA and the splenic cell chemotaxis mediated by mPVAT was evaluated using a transwell assay. In SPX mice, HFD induced adipocyte hypertrophy and increased immune cell infiltration and proinflammatory cytokine levels in mPVAT. However, none of these effects were observed in mPVAT from sham-operated mice. Spleen from HFD fed mice presented reduced total leukocytes and increased inflammatory markers when compared to the spleen from control mice. Chemotaxis of spleen cells mediated by mPVAT of HFD fed mice was reduced in relation to standard diet fed mice. The spleen protects mPVAT against the effects of 16-week HFD. This information was missing, and it is important because PVAT is different from other fat depots and data cannot be extrapolated from any type of adipose tissue to PVAT.

Perivascular adipose tissue, inflammation and insulin resistance: link to vascular dysfunction and cardiovascular disease

2015 ◽  
Vol 22 (1) ◽  
Author(s):  
Guido Lastra ◽  
Camila Manrique
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Small Diameter ◽  
Perivascular Adipose Tissue ◽  
Anti Inflammatory ◽  
Visceral Adipose

AbstractObesity is a leading risk factor for the development of type 2 diabetes mellitus (DM2) and cardiovascular disease (CVD), however the underlying mechanisms still remain to be fully uncovered. It is now well accepted that dysfunctional adipose tissue in conditions of obesity is a critical source of inflammation that impacts the cardiovascular system and contributes to CVD. Although traditionally visceral adipose tissue has been linked to increased CVD risk, there is mounting interest in the role that fat accumulation around the vasculature plays in the pathogenesis of vascular dysfunction. Perivascular adipose tissue (PVAT) is in intimate contact with large, medium and small diameter arterial beds in several tissues, and has been shown to control vascular function as well as remodeling. PVAT does not merely mirror visceral adipose tissue changes seen in obesity, but has unique features that impact vascular biology. In lean individuals PVAT exerts vasodilatory and anti-inflammatory functions, however obesity results in PVAT inflammation, characterized by imbalance between pro- and anti-inflammatory cells as wells as adipokines. PVAT inflammation promotes insulin resistance in the vasculature, thus resulting in impaired insulin-mediated vasodilatory responses and vascular remodeling. In this review we address current knowledge about the mechanisms that link PVAT inflammation to insulin resistance and vascular dysfunction. Indeed, PVAT emerges as a novel type of adipose tissue that participates in the pathogenesis of CVD, independently to a large extent to visceral adipose tissue.

scholarly journals The role of perivascular adipose tissue in vasoconstriction, arterial stiffness, and aneurysm

2015 ◽  
Vol 21 (2) ◽  
Author(s):  
Luis Villacorta ◽  
Lin Chang
Keyword(s):  
Adipose Tissue ◽  
Arterial Stiffness ◽  
Vascular Function ◽  
Molecular Mechanisms ◽  
Inflammatory Cells ◽  
Phenotypic Change ◽  
Neointimal Formation ◽  
Perivascular Adipose Tissue ◽  
Fat Depots ◽  
Brown Adipose

AbstractSince the “rediscovery” of brown adipose tissue in adult humans, significant scientific efforts are being pursued to identify the molecular mechanisms to promote a phenotypic change of white adipocytes into brown-like cells, a process called “browning”. It is well documented that white adipose tissue (WAT) mass and factors released from WAT influence the vascular function and positively correlate with cardiac arrest, stroke, and other cardiovascular complications. Similar to other fat depots, perivascular adipose tissue (PVAT) is an active endocrine organ and anatomically surrounds vessels. Both brown-like and white-like PVAT secrete various adipokines, cytokines, and growth factors that either prevent or promote the development of cardiovascular diseases (CVDs) depending on the relative abundance of each type and their bioactivity in the neighboring vasculature. Notably, pathophysiological conditions, such as obesity, hypertension, or diabetes, induce the imbalance of PVAT-derived vasoactive products that promote the infiltration of inflammatory cells. This then triggers derangements in vascular smooth muscle cells and endothelial cell dysfunction, resulting in the development of vascular diseases. In this review, we discuss the recent advances on the contribution of PVAT in CVDs. Specifically, we summarize the current proposed roles of PVAT in relationship with vascular contractility, endothelial dysfunction, neointimal formation, arterial stiffness, and aneurysm.

scholarly journals Perivascular Adipose Tissue Regulates Vascular Function by Targeting Vascular Smooth Muscle Cells

2020 ◽  
Vol 40 (5) ◽  
pp. 1094-1109 ◽  
Author(s):  
Lin Chang ◽  
Minerva T. Garcia-Barrio ◽  
Y. Eugene Chen
Keyword(s):  
Adipose Tissue ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Function ◽  
Muscle Cells ◽  
The Body ◽  
Adipose Tissues ◽  
Perivascular Adipose Tissue

Adipose tissues are present at multiple locations in the body. Most blood vessels are surrounded with adipose tissue which is referred to as perivascular adipose tissue (PVAT). Similarly to adipose tissues at other locations, PVAT harbors many types of cells which produce and secrete adipokines and other undetermined factors which locally modulate PVAT metabolism and vascular function. Uncoupling protein-1, which is considered as a brown fat marker, is also expressed in PVAT of rodents and humans. Thus, compared with other adipose tissues in the visceral area, PVAT displays brown-like characteristics. PVAT shows a distinct function in the cardiovascular system compared with adipose tissues in other depots which are not adjacent to the vascular tree. Growing and extensive studies have demonstrated that presence of normal PVAT is required to maintain the vasculature in a functional status. However, excessive accumulation of dysfunctional PVAT leads to vascular disorders, partially through alteration of its secretome which, in turn, affects vascular smooth muscle cells and endothelial cells. In this review, we highlight the cross talk between PVAT and vascular smooth muscle cells and its roles in vascular remodeling and blood pressure regulation.

Obesity, Adipose Tissue and Vascular Dysfunction

2021 ◽  
Vol 128 (7) ◽  
pp. 951-968 ◽  
Author(s):  
Mascha Koenen ◽  
Michael A. Hill ◽  
Paul Cohen ◽  
James R. Sowers
Keyword(s):  
Adipose Tissue ◽  
Cardiovascular Diseases ◽  
Vascular Function ◽  
Cardiovascular Health ◽  
Immune Cell ◽  
Vascular Dysfunction ◽  
The United States ◽  
Overweight And Obesity ◽  
Perivascular Adipose Tissue ◽  
Adipose Tissue Depots

Cardiovascular diseases are the leading cause of death worldwide. Overweight and obesity are strongly associated with comorbidities such as hypertension and insulin resistance, which collectively contribute to the development of cardiovascular diseases and resultant morbidity and mortality. Forty-two percent of adults in the United States are obese, and a total of 1.9 billion adults worldwide are overweight or obese. These alarming numbers, which continue to climb, represent a major health and economic burden. Adipose tissue is a highly dynamic organ that can be classified based on the cellular composition of different depots and their distinct anatomical localization. Massive expansion and remodeling of adipose tissue during obesity differentially affects specific adipose tissue depots and significantly contributes to vascular dysfunction and cardiovascular diseases. Visceral adipose tissue accumulation results in increased immune cell infiltration and secretion of vasoconstrictor mediators, whereas expansion of subcutaneous adipose tissue is less harmful. Therefore, fat distribution more than overall body weight is a key determinant of the risk for cardiovascular diseases. Thermogenic brown and beige adipose tissue, in contrast to white adipose tissue, is associated with beneficial effects on the vasculature. The relationship between the type of adipose tissue and its influence on vascular function becomes particularly evident in the context of the heterogenous phenotype of perivascular adipose tissue that is strongly location dependent. In this review, we address the abnormal remodeling of specific adipose tissue depots during obesity and how this critically contributes to the development of hypertension, endothelial dysfunction, and vascular stiffness. We also discuss the local and systemic roles of adipose tissue derived secreted factors and increased systemic inflammation during obesity and highlight their detrimental impact on cardiovascular health.

scholarly journals Role of Inflammation in Vascular Disease-Related Perivascular Adipose Tissue Dysfunction

2021 ◽  
Vol 12 ◽  
Author(s):  
Yaozhi Chen ◽  
Zeyu Qin ◽  
Yaqiong Wang ◽  
Xin Li ◽  
Yang Zheng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Blood Vessels ◽  
Vascular Inflammation ◽  
Vascular Diseases ◽  
The Body ◽  
Vascular Aging ◽  
Perivascular Adipose Tissue ◽  
Free Fatty Acid Metabolism ◽  
Anti Inflammatory

Perivascular adipose tissue (PVAT) is the connective tissue around most blood vessels throughout the body. It provides mechanical support and maintains vascular homeostasis in a paracrine/endocrine manner. Under physiological conditions, PVAT has anti-inflammatory effects, improves free fatty acid metabolism, and regulates vasodilation. In pathological conditions, PVAT is dysfunctional, secretes many anti-vasodilator factors, and participates in vascular inflammation through various cells and mediators; thus, it causes dysfunction involving vascular smooth muscle cells and endothelial cells. Inflammation is an important pathophysiological event in many vascular diseases, such as vascular aging, atherosclerosis, and hypertension. Therefore, the pro-inflammatory crosstalk between PVAT and blood vessels may comprise a novel therapeutic target for the prevention and treatment of vascular diseases. In this review, we summarize findings concerning PVAT function and inflammation in different pathophysiological backgrounds, focusing on the secretory functions of PVAT and the crosstalk between PVAT and vascular inflammation in terms of vascular aging, atherosclerosis, hypertension, diabetes mellitus, and other diseases. We also discuss anti-inflammatory treatment for potential vascular diseases involving PVAT.

scholarly journals Perivascular adipose tissue modulates vascular function in the human internal thoracic artery

2005 ◽  
Vol 130 (4) ◽  
pp. 1130-1136 ◽  
Author(s):  
Yu-Jing Gao ◽  
Zhao-hua Zeng ◽  
Kevin Teoh ◽  
Arya M. Sharma ◽  
Labib Abouzahr ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Vascular Function ◽  
Internal Thoracic Artery ◽  
Perivascular Adipose Tissue

scholarly journals Maternal separation enhances anticontractile perivascular adipose tissue function in male rats on a high-fat diet

2018 ◽  
Vol 315 (6) ◽  
pp. R1085-R1095 ◽  
Author(s):  
Analia S. Loria ◽  
Frank T. Spradley ◽  
Ijeoma E. Obi ◽  
Bryan K. Becker ◽  
Carmen De Miguel ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Life Stress ◽  
Vascular Function ◽  
Maternal Separation ◽  
Male Rats ◽  
Protective Effects ◽  
Ang Ii ◽  
High Fat ◽  
Perivascular Adipose Tissue

Clinical studies have shown that obesity negatively impacts large arteries’ function. We reported that rats exposed to maternal separation (MatSep), a model of early life stress, display enhanced angiotensin II (ANG II)-induced vasoconstriction in aortic rings cleaned of perivascular adipose tissue (PVAT) under normal diet (ND) conditions. We hypothesized that exposure to MatSep promotes a greater loss of PVAT-mediated protective effects on vascular function and loss of blood pressure (BP) rhythm in rats fed a high-fat diet (HFD) when compared with controls. MatSep was performed in male Wistar-Kyoto rats from days 2 to 14 of life. Normally reared littermates served as controls. On ND, aortic rings from MatSep rats with PVAT removed showed increased ANG II-mediated vasoconstriction versus controls; however, rings from MatSep rats with intact PVAT displayed blunted constriction. This effect was exacerbated by an HFD in both groups; however, the anticontractile effect of PVAT was greater in MatSep rats. Acetylcholine-induced relaxation was similar in MatSep and control rats fed an ND, regardless of the presence of PVAT. HFD impaired aortic relaxation in rings without PVAT from MatSep rats, whereas the presence of PVAT improved relaxation in both groups. On an HFD, immunolocalization of vascular smooth muscle-derived ANG-(1–7) and PVAT-derived adiponectin abundances were increased in MatSep. In rats fed an HFD, 24-h BP and BP rhythms were similar between groups. In summary, MatSep enhanced the ability of PVAT to blunt the heightened ANG II-induced vasoconstriction and endothelial dysfunction in rats fed an HFD. This protective effect may be mediated via the upregulation of vasoprotective factors within the adipovascular axis.

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