scholarly journals Visceral adiposopathy: a vascular perspective

2015 ◽  
Vol 21 (2) ◽  
Author(s):  
Melissa G. Farb ◽  
Noyan Gokce
Keyword(s):  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Multiple Organ ◽  
Vascular Endothelial ◽  
Metabolic Dysfunction ◽  
Central Adiposity ◽  
Organ Systems ◽  
Tissue Characteristics ◽  
Care Problems ◽  
Visceral Adipose

AbstractObesity has emerged as one of the most critical health care problems globally that is associated with the development of insulin resistance, type 2 diabetes mellitus, metabolic dysfunction and cardiovascular disease. Central adiposity with intra-abdominal deposition of visceral fat, in particular, has been closely linked to cardiometabolic consequences of obesity. Increasing epidemiological, clinical and experimental data suggest that both adipose tissue quantity and perturbations in its quality termed “adiposopathy” contribute to mechanisms of cardiometabolic disease. The current review discusses regional differences in adipose tissue characteristics and highlights profound abnormalities in vascular endothelial function and angiogenesis that are manifest within the visceral adipose tissue milieu of obese individuals. Clinical data demonstrate up-regulation of pro-inflammatory and pro-atherosclerotic mediators in dysfunctional adipose tissue that may support pathological vascular changes not only locally in fat but also in multiple organ systems, including coronary and peripheral circulations, potentially contributing to mechanisms of obesity-related cardiovascular disease.

scholarly journals Role of Arginase 2 in Systemic Metabolic Activity and Adipose Tissue Fatty Acid Metabolism in Diet-Induced Obese Mice

2019 ◽  
Vol 20 (6) ◽  
pp. 1462 ◽  
Author(s):  
Reem Atawia ◽  
Haroldo Toque ◽  
Mohamed Meghil ◽  
Tyler Benson ◽  
Nicole Yiew ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Normal Diet ◽  
Metabolic Dysfunction ◽  
Ppar Γ ◽  
Obesity And Diabetes ◽  
Visceral Adipose ◽  
Upregulated Genes

Visceral adipose tissue (VAT) inflammation and metabolic dysregulation are key components of obesity-induced metabolic disease. Upregulated arginase, a ureahydrolase enzyme with two isoforms (A1-cytosolic and A2-mitochondrial), is implicated in pathologies associated with obesity and diabetes. This study examined A2 involvement in obesity-associated metabolic and vascular disorders. WT and globally deleted A2(−/−) or A1(+/−) mice were fed either a high fat/high sucrose (HFHS) diet or normal diet (ND) for 16 weeks. Increases in body and VAT weight of HFHS-fed WT mice were abrogated in A2−/−, but not A1+/−, mice. Additionally, A2−/− HFHS-fed mice exhibited higher energy expenditure, lower blood glucose, and insulin levels compared to WT HFHS mice. VAT and adipocytes from WT HFHS fed mice showed greater A2 expression and adipocyte size and reduced expression of PGC-1α, PPAR-γ, and adiponectin. A2 deletion blunted these effects, increased levels of active AMPK-α, and upregulated genes involved in fatty acid metabolism. A2 deletion prevented HFHS-induced VAT collagen deposition and inflammation, which are involved in adipocyte metabolic dysfunction. Endothelium-dependent vasorelaxation, impaired by HFHS diet, was significantly preserved in A2−/− mice, but more prominently maintained in A1+/− mice. In summary, A2 is critically involved in HFHS-induced VAT inflammation and metabolic dysfunction.

Cardiovascular Effects of Endothelin

Physiology ◽  
1997 ◽  
Vol 12 (3) ◽  
pp. 113-117
Author(s):  
JD Grossman ◽  
JP Morgan
Keyword(s):  
Endothelial Cells ◽  
Heart Disease ◽  
Vascular Endothelial Cells ◽  
Cardiovascular Effects ◽  
Multiple Organ ◽  
Vascular Endothelial ◽  
Cellular Calcium ◽  
Organ Systems

Endothelin is a potent vasoconstricting agent released by vascular endothelial cells. Endothelin affects multiple organ systems and occurs at high levels with heart disease. Changes in cellular calcium levels and Ca2+ sensitization of myofilaments mediate the endothelin pathway. The ability to modulate endothelin levels may lead to many effective therapies.

scholarly journals Autonomic and inflammatory consequences of posttraumatic stress disorder and the link to cardiovascular disease

2015 ◽  
Vol 309 (4) ◽  
pp. R315-R321 ◽  
Author(s):  
Chevelle Brudey ◽  
Jeanie Park ◽  
Jan Wiaderkiewicz ◽  
Ihori Kobayashi ◽  
Thomas A. Mellman ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Autonomic Dysfunction ◽  
Stress Disorder ◽  
Renin Angiotensin System ◽  
Multiple Organ ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Organ Systems

Stress- and anxiety-related disorders are on the rise in both military and general populations. Over the next decade, it is predicted that treatment of these conditions, in particular, posttraumatic stress disorder (PTSD), along with its associated long-term comorbidities, will challenge the health care system. Multiple organ systems are adversely affected by PTSD, and PTSD is linked to cancer, arthritis, digestive disease, and cardiovascular disease. Evidence for a strong link between PTSD and cardiovascular disease is compelling, and this review describes current clinical data linking PTSD to cardiovascular disease, via inflammation, autonomic dysfunction, and the renin-angiotensin system. Recent clinical and preclinical evidence regarding the role of the renin-angiotensin system in the extinction of fear memory and relevance in PTSD-related immune and autonomic dysfunction is also addressed.

The Systemic Effects of Endometriosis

2017 ◽  
Vol 35 (03) ◽  
pp. 263-270 ◽  
Author(s):  
Myles Alderman ◽  
Nicole Yoder ◽  
Hugh Taylor
Keyword(s):  
Cardiovascular Disease ◽  
Body Weight ◽  
Multiple Organ ◽  
Review Literature ◽  
Micro Rna ◽  
Systemic Effects ◽  
Stem Cell Migration ◽  
Treatment And Prevention ◽  
Organ Systems ◽  
Psychiatric Conditions

AbstractEndometriosis is a condition defined by the presence of endometrial glands and stroma in ectopic locations. While the most commonly seen symptoms of the disease are pelvic pain, dysmenorrhea, and infertility, endometriosis has also systemic effects in multiple organ systems. Here, we review literature describing closely associated comorbidities including cardiovascular disease, cancers, autoimmune disease, psychiatric conditions, and metabolism/body weight. We examine the pathophysiology and hypothesized mechanism by which endometriosis may lead to these systemic effects; mechanisms include cytokine and micro-RNA production as well as stem cell migration and dissemination. The broad systemic effects of endometriosis as well as correlated comorbidities are often overlooked in the treatment of patients with endometriosis. Increased awareness may lead to more effective treatment and prevention.

scholarly journals A TRAIL-TL1A paracrine network involving adipocytes, macrophages and lymphocytes induces adipose tissue dysfunction downstream of E2F1 in human obesity

2020 ◽  
Author(s):  
Ada Admin ◽  
Nitzan Maixner ◽  
Tal Pecht ◽  
Yulia Haim ◽  
Vered Chalifa-Caspi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Stromal Vascular Fraction ◽  
Metabolic Dysfunction ◽  
Trail Expression ◽  
Adipose Tissue Dysfunction ◽  
M1 Polarization ◽  
Tnf Superfamily ◽  
Diabetes Status ◽  
Elevated Expression ◽  
Visceral Adipose

Elevated expression of E2F1 in adipocyte-fraction of human visceral adipose-tissue(hVAT) associates with a poor cardio-metabolic profile. We hypothesized that beyond directly activating autophagy and MAP3K5(ASK)-MAP-kinase signaling, E2F1 governs a distinct transcriptome that contributes to adipose-tissue and metabolic dysfunction in obesity. We performed RNA-sequencing of hVAT samples from age-, sex- and BMI–matched patients, all obese, whose visceral-E2F1 protein expression was either high(E2F1<sup>high</sup>) or low(E2F1<sup>low</sup>). TNF-superfamily members, including <i>TRAIL</i>(<i>TNFSF10</i>), <i>TL1A</i>(<i>TNFSF15</i>) and their receptors were enriched in E2F1<sup>high</sup>. While <i>TRAIL</i> was equally expressed in adipocytes and stromal-vascular fraction(SVF), <i>TL1A </i>was mainly expressed in SVF, and TRAIL-induced <i>TL1A</i> was attributed to CD4+ and CD8<sup>+</sup>-subclasses of hVAT T-lymphocytes. In human adipocytes TL1A enhanced basal and impaired insulin-inhibitable lipolysis, and altered adipokine secretion, and in human macrophages induced foam-cells biogenesis and M1-polarization. Two independent human cohorts confirmed associations between TL1A and TRAIL expression in hVAT and higher leptin and IL6 serum concentrations, diabetes status, and hVAT-macrophage lipid content. Jointly, we propose an intra-adipose tissue E2F1-associated TNF-superfamily paracrine loop engaging lymphocytes, macrophages and adipocytes, ultimately contributing to adipose-tissue dysfunction in obesity.

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