Role of perivascular adipose tissue in endothelial dysfunction of adipose triglyceride lipase-deficient mice

Nitric Oxide ◽  
2012 ◽  
Vol 27 ◽  
pp. S21
Author(s):  
Karoline Dörffel ◽  
Sarah Winkler ◽  
Günter Hämmerle ◽  
Rudolf Zechner ◽  
Alois Lametschwandtner ◽  
...  
2012 ◽  
Vol 13 (S1) ◽  
Author(s):  
Karoline Pail ◽  
Sarah Winkler ◽  
Gerald Wölkart ◽  
Günter Hämmerle ◽  
Rudolf Zechner ◽  
...  

2013 ◽  
Vol 14 (S1) ◽  
Author(s):  
Marion Mussbacher ◽  
Karoline Pail ◽  
Gerald Wölkart ◽  
Günter Hämmerle ◽  
Alois Lametschwandtner ◽  
...  

2013 ◽  
Vol 37 ◽  
pp. S58 ◽  
Author(s):  
Camille Attané ◽  
Marie- Line Peyot ◽  
Shupei Wang ◽  
Grant A. Mitchell ◽  
Roxane Lussier ◽  
...  

2014 ◽  
Vol 77 ◽  
pp. 11-19 ◽  
Author(s):  
Marion Mussbacher ◽  
Heike Stessel ◽  
Gerald Wölkart ◽  
Guenter Haemmerle ◽  
Rudolf Zechner ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Osaki ◽  
Y Sato ◽  
S Endo ◽  
K Ito ◽  
K Kagami ◽  
...  

Abstract Introduction Extracellular signal-regulated kinase (ERK) modulates differentiation and maturation of adipocyte and the hypertrophy and differentiation of adipocytes affected the vascular diseases in obese. Changes in characters of adipocytes could develope the oxidative stress and inflammations. Moreover, changes in perivascular adipose tissue (PVAT) could modulate vascular tonus in obesity. However, the role of adipose ERK2 in endothelial function and characters of PVAT in obese in vivo had not been clarified, yet. Purpose This study aims to elucidate the role of the adipose ERK2 in endothelial-dependent relaxation (EDR) in mice model of obesity. The role of PVAT in EDR was also assessed. Methods and results We created adipose-specific ERK2 knock out mice (AE2KO) by crossing fatty acid binding protein 4 Cre and ERK2 flox mice and fed them with normal diet (ND) or high fat/ high sucrose diet (HFHSD) for 24 weeks. AE2KO fed with HFHSD gained more weight and revealed the heterogeneity in sizes of adipocyte in subcutaneous fat (SF). Furthermore, the mRNA levels of lipoprotein lipase, hormone-sensitive lipase, and peroxisome proliferator-activated receptor γ, which was the master genes of adipocyte differentiation, were markedly down-regulated in SF. PVAT in AE2KO with HFHSD was markedly enlarged and the mRNA expression of inflammatory adipocytokines, such as IL-1β and leptin were up-regulated. Next, we assessed EDR by acetylcholine (ACh) -induced relaxation in aortic rings with or without PVAT. EDR without PVAT was modestly decreased in AE2KO with HFHSD compared with wild type mice (WT) with HFHSD. Aortic rings with PVAT increased EDR in WT with ND. PVAT modestly decreased EDR in WT with HFHSD and mostly eliminated EDR in AE2KO with HFHSD. To assess the contraction factors released from PVAT, the solutions incubated with PVAT (SIP) were transferred to the normal aortic rings. SIP from WT with HFHSD mildly increased vascular tone and SIP from AE2KO with HFHSD further increased it. Tempol, which was superoxide scavenger, restored endothelial dysfunction with PVAT and suppressed the contraction with SIP from AE2KO with HFHSD. Fluorescence intensity of dihydroethidium stain of aorta and PVAT, which indicated that aortic and adipose superoxide production were elevated in AE2KO with HFHSD, which were mostly eliminated with tempol. Conclusions Adipose ERK2 selectively modulated differentiation in SF, suppressed the aortic oxidative stress and protected from endothelial dysfunction in obese. Moreover, adipose ERK2 suppressed the hypertrophy, inflammation, and oxidative stress of PVAT in obese. The oxidative stress with the inflammation in PVAT released vasoconstriction factors, which contributed to endothelial dysfunction in obese mice. Figure 1 Funding Acknowledgement Type of funding source: None


2007 ◽  
Vol 8 (1) ◽  
pp. 228
Author(s):  
M. Schweiger ◽  
G. Schoiswohl ◽  
A. Lass ◽  
G. Haemmerle ◽  
R. Zechner ◽  
...  

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Michael J. Trites ◽  
Robin D. Clugston

AbstractThe ability of mammals to store and draw on fat reserves has been a driving force throughout evolution in an environment with intermittent nutrient availability. The discovery of adipose triglyceride lipase (ATGL) as a triglyceride lipase provided a heightened understanding of the mechanisms governing mobilization of fat reserves from adipose tissue. ATGL catalyses the initial step in adipose triglyceride lipolysis, working in concert with other enzymes to mobilize triglyceride for energy production. In addition to the role of ATGL in adipose tissue triglyceride mobilization, ATGL plays crucial roles in regulating lipid homeostasis in other tissues. These roles have been characterized primarily using transgenic mice with tissue-specific ATGL ablation. For example, the global ATGL knockout induces a severe cardiac defect that results in premature mortality that is mimicked by inducible cardiomyocyte-specific ATGL knockout. Global- and adipose-specific ATGL ablation induces a whole-body shift from lipid metabolism to glucose metabolism to satisfy metabolic demand primarily facilitated by an increase in glucose uptake by skeletal muscle. Generation of liver-specific ATGL knockouts has implicated hepatic lipolysis as a critical component of normal liver function. Analysis of β-cell ATGL knockouts implicates the necessity of pancreatic ATGL in insulin secretion. The objective of this review is to discuss the contributions of ATGL to systemic lipid- and glucose-homeostasis discovered through the study of transgenic mice.


Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 613
Author(s):  
Valentina Rovella ◽  
Giuseppe Rodia ◽  
Francesca Di Daniele ◽  
Carmine Cardillo ◽  
Umberto Campia ◽  
...  

In the past few decades, obesity has reached pandemic proportions. Obesity is among the main risk factors for cardiovascular diseases, since chronic fat accumulation leads to dysfunction in vascular endothelium and to a precocious arterial stiffness. So far, not all the mechanisms linking adipose tissue and vascular reactivity have been explained. Recently, novel findings reported interesting pathological link between endothelial dysfunction with gut hormones and gut microbiota and energy homeostasis. These findings suggest an active role of gut secretome in regulating the mediators of vascular function, such as nitric oxide (NO) and endothelin-1 (ET-1) that need to be further investigated. Moreover, a central role of brain has been suggested as a main player in the regulation of the different factors and hormones beyond these complex mechanisms. The aim of the present review is to discuss the state of the art in this field, by focusing on the processes leading to endothelial dysfunction mediated by obesity and metabolic diseases, such as insulin resistance. The role of perivascular adipose tissue (PVAT), gut hormones, gut microbiota dysbiosis, and the CNS function in controlling satiety have been considered. Further understanding the crosstalk between these complex mechanisms will allow us to better design novel strategies for the prevention of obesity and its complications.


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