Faculty Opinions recommendation of Perivascular adipose tissue and its role in type 2 diabetes and cardiovascular disease.

Author(s):  
Rosemarie Heyn
2011 ◽  
Vol 11 (3) ◽  
pp. 211-217 ◽  
Author(s):  
Rick I. Meijer ◽  
Erik H. Serne ◽  
Yvo M. Smulders ◽  
Victor W. M. van Hinsbergh ◽  
John S. Yudkin ◽  
...  

Author(s):  
Preeti Sharma ◽  
Shailaza Shrestha ◽  
Pradeep Kumar ◽  
Saxena Sp ◽  
Rachna Sharma

ABSTRACTAmong the adipokines, adiponectin is the first one to be described just over a decade ago. It is produced exclusively by adipose tissue and circulatesin high concentration in human plasma accounting for 0.01% of proteins in plasma, almost thousand times higher than that of leptin. The normalcirculating level of adiponectin ranges from 2 to 30 µg/ml. It is now observed that besides adipose tissue, adiponectin can also be produced byseveral other tissues such as hepatocytes, cardiomyocytes, and placenta. Adiponectin executes its action via autocrine as well as and paracrine effects.Researchers working in this area have revealed that adiponectin has insulin-sensitizing, anti-inflammatory and cardioprotective effects. Our reviewfocuses on adiponectin, its mode of action on different peripheral tissues such as skeletal muscles, heart, liver, brain and its the correlative accountin various diseases.Keywords: Adiponectin, Obesity, Type 2 diabetes, Inflammation, Malignancies, Cardiovascular disease.


2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Regitse H. Christensen ◽  
Bernt Johan von Scholten ◽  
Christian S. Hansen ◽  
Magnus T. Jensen ◽  
Tina Vilsbøll ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Saxton ◽  
R J Potter ◽  
S B Withers ◽  
R Grencis ◽  
A M Heagerty

Abstract Background/Purpose Perivascular adipose tissue (PVAT) is essential in the modulation of vascular tone. Recently we have shown that resident eosinophils play a vital role in regulating PVAT function. In obesity, eosinophil numbers are reduced and PVAT anticontractile function is lost, resulting in increased vascular tone, which will contribute to development of hypertension and type-2 diabetes. Evidence suggests that eosinophilia resulting from parasitic infection may be useful in improving glucose tolerance; therefore, we investigated the effects of eosinophilia on PVAT function in health and obesity. Methods Control mice and a high fat fed mouse model of obesity were administered intraperitoneal injections of interleukin-33 (IL-33, 0.1μg) over a five day period. Blood pressure, blood glucose and plasma insulin were measured and compared with un-injected control and obese mice. Wire myography was used to assess the vascular contractility of mesenteric arteries (<250μm, +/− PVAT) from both injected and un-injected control and obese mice in response to noradrenaline. ELISAs and immunohistochemistry were used to examine eosinophil numbers. Results High fat feeding induced significant elevations in blood pressure, blood glucose and plasma insulin, which were reduced using IL-33 injections. Eosinophilia was confirmed in blood plasma using an eosinophil cationic protein ELISA. Using wire myography, mesenteric arteries from control mice PVAT exerted an anticontractile effect on the vessels, which was enhanced in control mice injected with IL-33. In obese mice, the PVAT anticontractile effect was lost, but was restored in IL-33 injected obese mice. Using immunohistochemistry, we confirm that eosinophils numbers in PVAT were reduced in obesity and increased in IL-33 treated PVAT. Conclusions IL-33 injections induced eosinophilia in both control and obese mice. IL-33 treatment restored PVAT function in obesity, and enhanced the anticontractile function of PVAT in healthy animals. In addition, only five consecutive injections of IL-33 reversed development of hypertension and type-2 diabetes in obese mice. These data suggest that IL-33 induced eosinophilia presents a novel approach to treatment of hypertension and type-2 diabetes in obesity. Acknowledgement/Funding British Heart Foundation


2018 ◽  
Vol 120 ◽  
pp. S162 ◽  
Author(s):  
Adriana Leandro ◽  
Lara Azul ◽  
Rosa Fernandes ◽  
Raquel Seiça ◽  
Cristina Sena

2021 ◽  
Vol 22 (24) ◽  
pp. 13671
Author(s):  
Marcelo Queiroz ◽  
Adriana Leandro ◽  
Lara Azul ◽  
Artur Figueirinha ◽  
Raquel Seiça ◽  
...  

We investigated the effects of luteolin on metabolism, vascular reactivity, and perivascular adipose tissue (PVAT) in nonobese type 2 diabetes mellitus animal model, Goto-Kakizaki (GK) rats. Methods: Wistar and GK rats were divided in two groups: (1) control groups treated with vehicle; (2) groups treated with luteolin (10 mg/kg/day, for 2 months). Several metabolic parameters such as adiposity index, lipid profile, fasting glucose levels, glucose and insulin tolerance tests were determined. Endothelial function and contraction studies were performed in aortas with (PVAT+) or without (PVAT−) periaortic adipose tissue. We also studied vascular oxidative stress, glycation and assessed CRP, CCL2, and nitrotyrosine levels in PVAT. Results: Endothelial function was impaired in diabetic GK rats (47% (GK − PVAT) and 65% (GK + PVAT) inhibition of maximal endothelial dependent relaxation) and significantly improved by luteolin treatment (29% (GK − PVAT) and 22% (GK + PVAT) inhibition of maximal endothelial dependent relaxation, p < 0.01). Vascular oxidative stress and advanced glycation end-products’ levels were increased in aortic rings (~2-fold, p < 0.05) of diabetic rats and significantly improved by luteolin treatment (to levels not significantly different from controls). Periaortic adipose tissue anti-contractile action was significantly rescued with luteolin administration (p < 0.001). In addition, luteolin treatment significantly recovered proinflammatory and pro-oxidant PVAT phenotype, and improved systemic and metabolic parameters in GK rats. Conclusions: Luteolin ameliorates endothelial dysfunction in type 2 diabetes and exhibits therapeutic potential for the treatment of vascular complications associated with type 2 diabetes.


Author(s):  
Jennifer Honek ◽  
Sharon Lim ◽  
Carina Fischer ◽  
Hideki Iwamoto ◽  
Takahiro Seki ◽  
...  

AbstractThe number of obese and overweight individuals is globally rising, and obesity-associated disorders such as type 2 diabetes, cardiovascular disease and certain types of cancer are among the most common causes of death. While white adipose tissue is the key player in the storage of energy, active brown adipose tissue expends energy due to its thermogenic capacity. Expanding and activating brown adipose tissue using pharmacological approaches therefore might offer an attractive possibility for therapeutic intervention to counteract obesity and its consequences for metabolic health.


2020 ◽  
Vol 11 ◽  
pp. 204201882092882 ◽  
Author(s):  
Regitse Højgaard Christensen ◽  
Bernt Johan von Scholten ◽  
Louise Lang Lehrskov ◽  
Peter Rossing ◽  
Peter Godsk Jørgensen

Type 2 diabetes (T2D) is associated with an increased risk of cardiovascular disease and heart failure, which highlights the need for improved understanding of factors contributing to the pathophysiology of these complications as they are the leading cause of mortality in T2D. Patients with T2D have high levels of epicardial adipose tissue (EAT). EAT is known to secrete inflammatory factors, lipid metabolites, and has been proposed to apply mechanical stress on the cardiac muscle that may accelerate atherosclerosis, cardiac remodeling, and heart failure. High levels of EAT in patients with T2D have been associated with atherosclerosis, diastolic dysfunction, and incident cardiovascular events, and this fat depot has been suggested as an important link coupling diabetes, obesity, and cardiovascular disease. Despite this, the predictive potential of EAT in general, and in patients with diabetes, is yet to be established, and, up until now, the clinical relevance of EAT is therefore limited. Should this link be established, importantly, studies show that this fat depot can be modified both by pharmacological and lifestyle interventions. In this review, we first introduce the role of adipose tissue in T2D and present mechanisms involved in the pathophysiology of EAT and pericardial adipose tissue (PAT) in general, and in patients with T2D. Next, we summarize the evidence that these fat depots are elevated in patients with T2D, and discuss whether they might drive the high cardiometabolic risk in patients with T2D. Finally, we discuss the clinical potential of cardiac adipose tissues, address means to target this depot, and briefly touch upon underlying mechanisms and future research questions.


Diabetes ◽  
2015 ◽  
Vol 64 (6) ◽  
pp. 1904-1906 ◽  
Author(s):  
Jaume Padilla ◽  
Victoria J. Vieira-Potter ◽  
Guanghong Jia ◽  
James R. Sowers

2007 ◽  
Vol 85 (1) ◽  
pp. 113-132 ◽  
Author(s):  
Kerry B. Goralski ◽  
Christopher J. Sinal

The increasing national prevalence of obesity is a major public health concern and a substantial burden on the health care resources of Canada. In addition to the direct health impact of obesity, this condition is a well-established risk factor for the development of various prevalent comorbidities including type 2 diabetes, hypertension, and cardiovascular disease. Historically, adipose tissue has been regarded primarily as an organ for energy storage. However, the discovery of leptin in the mid 1990’s revolutionized our understanding of this tissue and has focused attention on the endocrine function of adipose tissue as a source of secreted bioactive peptides. These compounds, collectively termed adipokines, regulate a number of biological functions including appetite and energy balance, insulin sensitivity, lipid metabolism, blood pressure, and inflammation. The physiological importance of adipokines has led to the hypothesis that changes in the synthesis and secretion of these compounds in the obese are a causative factor contributing to the development of obesity and obesity-related diseases in these individuals. Following from this it has been proposed that pharmacologic manipulation of adipokine levels may provide novel effective therapeutic strategies to treat and prevent obesity, type 2 diabetes, and cardiovascular disease.


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