scholarly journals Acute hyperglycemia impairs flow-mediated dilatation through an increase in vascular oxidative stress: winter is coming for excess sugar consumption

2016 ◽  
Vol 8 (9) ◽  
pp. E1103-E1105
Author(s):  
Cindy Meziat ◽  
Jordan Loader ◽  
Cyril Reboul ◽  
Guillaume Walther
2017 ◽  
Vol 61 (11) ◽  
pp. 1700373 ◽  
Author(s):  
Arrigo F.G. Cicero ◽  
Cristiana Caliceti ◽  
Federica Fogacci ◽  
Marina Giovannini ◽  
Donato Calabria ◽  
...  

Author(s):  
Marco Orlandi ◽  
Stefano Masi ◽  
Devina Bhowruth ◽  
Yago Leira ◽  
Georgios Georgiopoulos ◽  
...  

Objective: Inflammation, oxidative stress, and endothelial dysfunction are known to contribute to ischemia-reperfusion injury. Remote ischemic preconditioning (RIPC) protects from endothelial dysfunction and the damage induced by ischemia-reperfusion. Using intensive periodontal treatment (IPT), an established human model of acute systemic inflammation, we investigated whether RIPC prevents endothelial dysfunction and modulates systemic levels of inflammation and oxidative stress. Approach and Results: Forty-nine participants with periodontitis were randomly allocated to receive either 3 cycles of ischemia-reperfusion on the upper limb (N=25, RIPC) or a sham procedure (N=24, control) before IPT. Endothelial function assessed by flow-mediated dilatation of the brachial artery, inflammatory cytokines, markers of vascular injury, and oxidative stress were evaluated at baseline, day 1, and day 7 after IPT. Twenty-four hours post-IPT, the RIPC group had lower levels of IL (interleukin)-10 and IL-12 compared with the control group ( P <0.05). RIPC attenuated the IPT-induced increase in IL-1β, E-selectin, sICAM-3 (soluble intercellular adhesion molecule 3), and s-thrombomodulin levels between the baseline and day 1 ( P for interaction <0.1). Conversely, oxidative stress was differentially increased at day1 in the RIPC group compared with the control group ( P for interaction <0.1). This was accompanied by a better flow-mediated dilatation (mean difference 1.75% [95% CI, 0.428–3.07], P =0.011). After 7 days from IPT, most of the inflammatory markers endothelial-dependent and -independent vasodilation were similar between groups. Conclusions: RIPC prevented acute endothelial dysfunction by modulation of inflammation and oxidation processes in patients with periodontitis following exposure to an acute inflammatory stimulus. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03072342.


2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Zsuzsanna Orosz ◽  
Anna Csiszar ◽  
Nazar Labinskyy ◽  
Kira Smith ◽  
Aracelie Rivera ◽  
...  

2011 ◽  
Vol 66A (8) ◽  
pp. 866-875 ◽  
Author(s):  
Z. Ungvari ◽  
L. Bailey-Downs ◽  
T. Gautam ◽  
D. Sosnowska ◽  
M. Wang ◽  
...  

2019 ◽  
Vol 20 (3) ◽  
pp. 499 ◽  
Author(s):  
Michela Zanetti ◽  
Gianluca Gortan Cappellari ◽  
Andrea Graziani ◽  
Rocco Barazzoni

Unacylated ghrelin (UnGhr) exerts several beneficial actions on vascular function. The aim of this study was to assess the effects of UnGhr on high-fat induced endothelial dysfunction and its underlying mechanisms. Thoracic aortas from transgenic mice, which were overexpressing UnGhr and being control fed either a standard control diet (CD) or a high-fat diet (HFD) for 16 weeks, were harvested and used for the assessment of vascular reactivity, endothelial nitric oxide synthase (eNOS) expression and activity, thiobarbituric acid reactive substances (TBARS) and glutathione levels, and aortic lipid accumulation by Oil Red O staining. Relaxations due to acetylcholine and to DEA-NONOate were reduced (p < 0.05) in the HFD control aortas compared to vessels from the CD animals. Overexpression of UnGhr prevented HFD-induced vascular dysfunction, while eNOS expression and activity were similar in all vessels. HFD-induced vascular oxidative stress was demonstrated by increased (p < 0.05) aortic TBARS and glutathione in wild type (Wt) mice; however, this was not seen in UnGhr mice. Moreover, increased (p < 0.05) HFD-induced lipid accumulation in vessels from Wt mice was prevented by UnGhr overexpression. In conclusion, chronic UnGhr overexpression results in improved vascular function and reduced plaque formation through decreased vascular oxidative stress, without affecting the eNOS pathway. This research may provide new insight into the mechanisms underlying the beneficial effects of UnGhr on the vascular dysfunction associated with obesity and the metabolic syndrome.


2015 ◽  
Vol 32 (7) ◽  
pp. 687-698 ◽  
Author(s):  
Ece Sari ◽  
Yeliz Tunc-Sarisozen ◽  
Hulya Mutlu ◽  
Reza Shahbazi ◽  
Gulberk Ucar ◽  
...  

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