46-LB: Exercise Improves Endothelial Function Associated with Alleviated Inflammation and Oxidative Stress of Perivascular Adipose Tissue in Type 2 Diabetic Mice

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 46-LB
Author(s):  
JINJU WANG ◽  
VENKATA POLAKI ◽  
SHUZHEN CHEN ◽  
JI BIHL
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Endothelial Function ◽  
Diabetic Mice ◽  
Perivascular Adipose Tissue ◽  
And Oxidative Stress ◽  
Type 2 Diabetic

scholarly journals Exercise training improves endothelial function via adiponectin-dependent and independent pathways in type 2 diabetic mice

2011 ◽  
Vol 301 (2) ◽  
pp. H306-H314 ◽  
Author(s):  
Sewon Lee ◽  
Yoonjung Park ◽  
Kevin C. Dellsperger ◽  
Cuihua Zhang
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Exercise Training ◽  
Endothelial Function ◽  
Protein Expression ◽  
Diabetic Mice ◽  
Ifn Γ ◽  
And Oxidative Stress ◽  
Type 2 Diabetic

Type 2 diabetes (T2D) is a leading risk factor for a variety of cardiovascular diseases including coronary heart disease and atherosclerosis. Exercise training (ET) has a beneficial effect on these disorders, but the basis for this effect is not fully understood. This study was designed to investigate whether the ET abates endothelial dysfunction in the aorta in T2D. Heterozygous controls (m Lepr db) and type 2 diabetic mice ( db/db; Lepr db) were either exercise entrained by forced treadmill exercise or remained sedentary for 10 wk. Ex vivo functional assessment of aortic rings showed that ET restored acetylcholine-induced endothelial-dependent vasodilation of diabetic mice. Although the protein expression of endothelial nitric oxide synthase did not increase, ET reduced both IFN-γ and superoxide production by inhibiting gp91phox protein levels. In addition, ET increased the expression of adiponectin (APN) and the antioxidant enzyme, SOD-1. To investigate whether these beneficial effects of ET are APN dependent, we used adiponectin knockout (APNKO) mice. Indeed, impaired endothelial-dependent vasodilation occurred in APNKO mice, suggesting that APN plays a central role in prevention of endothelial dysfunction. APNKO mice also showed increased protein expression of IFN-γ, gp91phox, and nitrotyrosine but protein expression of SOD-1 and -3 were comparable between wild-type and APNKO. These findings in the aorta imply that APN suppresses inflammation and oxidative stress in the aorta, but not SOD-1 and -3. Thus ET improves endothelial function in the aorta in T2D via both APN-dependent and independent pathways. This improvement is due to the effects of ET in inhibiting inflammation and oxidative stress (APN-dependent) as well as in improving antioxidant enzyme (APN-independent) performance in T2D.

Serum Biomarker Measurements of Endothelial Function and Oxidative Stress After Daily Dosing of Sildenafil in Type 2 Diabetic Men With Erectile Dysfunction

2009 ◽  
Vol 181 (1) ◽  
pp. 245-251 ◽  
Author(s):  
Arthur L. Burnett ◽  
Travis D. Strong ◽  
Bruce J. Trock ◽  
Liming Jin ◽  
Trinity J. Bivalacqua ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Erectile Dysfunction ◽  
Endothelial Function ◽  
Serum Biomarker ◽  
And Oxidative Stress ◽  
Type 2 Diabetic

scholarly journals Luteolin Improves Perivascular Adipose Tissue Profile and Vascular Dysfunction in Goto-Kakizaki Rats

2021 ◽  
Vol 22 (24) ◽  
pp. 13671
Author(s):  
Marcelo Queiroz ◽  
Adriana Leandro ◽  
Lara Azul ◽  
Artur Figueirinha ◽  
Raquel Seiça ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Endothelial Function ◽  
Metabolic Parameters ◽  
Perivascular Adipose Tissue ◽  
Gk Rats ◽  
Vascular Oxidative Stress ◽  
Luteolin Treatment

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.

scholarly journals Effect of Quamoclit angulata Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 459 ◽  
Author(s):  
Ji Eun Park ◽  
Heaji Lee ◽  
Hyunkyung Rho ◽  
Seong Min Hong ◽  
Sun Yeou Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nlrp3 Inflammasome ◽  
High Fat Diet ◽  
Renal Damage ◽  
Model Assessment ◽  
Diabetic Mice ◽  
Homeostasis Model Assessment ◽  
And Oxidative Stress ◽  
Type 2 Diabetic

Type 2 diabetes mellitus (T2DM) is caused by abnormalities of controlling blood glucose and insulin homeostasis. Especially, hyperglycemia causes hyper-inflammation through activation of NLRP3 inflammasome, which can lead to cell apoptosis, hypertrophy, and fibrosis. Quamoclit angulata (QA), one of the annual winders, has been shown ameliorative effects on diabetes. The current study investigated whether the QA extract (QAE) attenuated hyperglycemia-induced renal inflammation related to NLRP inflammasome and oxidative stress in high fat diet (HFD)-induced diabetic mice. After T2DM was induced, the mice were treated with QAE (5 or 10 mg/kg/day) by gavage for 12 weeks. The QAE supplementation reduced homeostasis model assessment insulin resistance (HOMA-IR), kidney malfunction, and glomerular hypertrophy in T2DM. Moreover, the QAE treatment significantly attenuated renal NLRP3 inflammasome dependent hyper-inflammation and consequential renal damage caused by oxidative stress, apoptosis, and fibrosis in T2DM. Furthermore, QAE normalized aberrant energy metabolism (downregulation of p-AMPK, sirtuin (SIRT)-1, and PPARγ-coactivator α (PGC-1 α)) in T2DM mice. Taken together, the results suggested that QAE as a natural product has ameliorative effects on renal damage by regulation of oxidative stress and inflammation in T2DM.

scholarly journals Exercise Improves Endothelial Function Associated with Alleviated Inflammation and Oxidative Stress of Perivascular Adipose Tissue in Type 2 Diabetic Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Jinju Wang ◽  
Venkata Polaki ◽  
Shuzhen Chen ◽  
Ji C. Bihl
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Adipose Tissue ◽  
Endothelial Function ◽  
Exercise Intervention ◽  
Macrophage Polarization ◽  
Fasting Blood Glucose ◽  
Vascular Wall ◽  
Perivascular Adipose Tissue ◽  
And Oxidative Stress

Perivascular adipose tissue (PVAT), a type of adipose tissue that surrounds the blood vessels, has been considered an active component of the blood vessel walls and involved in vascular homeostasis. Recent evidence shows that increased inflammation and oxidative stress in PVAT contribute to endothelial dysfunction in type 2 diabetes (T2D). Exercise is an important nonpharmacological approach for vascular diseases. However, there is limited information regarding whether the beneficial effects of exercise on vascular function is related to the PVAT status. In this study, we investigated whether exercise can decrease oxidative stress and inflammation of PVAT and promote the improvement of endothelial function in a T2D mouse model. Diabetic db/db (5-week old) mice performed treadmill exercise (10 m/min) or keep sedentary for 8 weeks. Body weight, fasting blood glucose levels, glucose, and insulin tolerance were determined. The cytokines (IL-6, IL-10, IFN-γ, and TNF-a) and adiponectin levels, macrophage polarization and adipocyte type in PVAT, oxidative stress, and nitric oxide (NO) expression in the vascular wall were evaluated. The adhesion ability of primary aorta endothelial cells was analyzed. Our data showed that (1) diabetic db/db mice had increased body weight and fasting blood glucose level, compromised glucose tolerance, and insulin sensitivity, which were decreased/improved by exercise intervention. (2) Exercise intervention increased the percentage of multilocular brown adipocytes, promoted M1 to M2 macrophage polarization, associating with an increase of adiponectin and IL-10 levels and decrease of IFN-γ, IL-6, and TNF-a levels in PVAT. (3) Exercise decreased superoxide production in PVAT and the vascular wall of diabetic mice, accompanied with increased NO level. (4) The adhesion ability of aorta endothelial cells to leukocytes was decreased in exercised db/db mice, accompanied by decreased intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) expressions. Of interesting, coculture with PVAT-culture medium from exercised db/db mice could also reduce ICAM-1 and VCAM-1 expressions in primary endothelial cells. In conclusion, our data suggest that exercise improved endothelial function by attenuating the inflammation and oxidative stress in PVAT.

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