Dairy milk proteins attenuate hyperglycemia-induced impairments in vascular endothelial function in adults with prediabetes by limiting increases in glycemia and oxidative stress that reduce nitric oxide bioavailability

2019 ◽  
Vol 63 ◽  
pp. 165-176 ◽  
Author(s):  
Joshua D. McDonald ◽  
Eunice Mah ◽  
Chureeporn Chitchumroonchokchai ◽  
Priyankar Dey ◽  
Allison N. Labyk ◽  
...  
Aging ◽  
2017 ◽  
Vol 9 (1) ◽  
pp. 187-208 ◽  
Author(s):  
Jessica R. Santos-Parker ◽  
Talia R. Strahler ◽  
Candace J. Bassett ◽  
Nina Z. Bispham ◽  
Michel B. Chonchol ◽  
...  

2005 ◽  
Vol 30 (4) ◽  
pp. 442-474 ◽  
Author(s):  
James W.E. Rush ◽  
Steven G. Denniss ◽  
Drew A. Graham

Cardiovascular disease is the single leading cause of death and morbidity for Canadians. A universal feature of cardiovascular disease is dysfunction of the vascular endothelium, thus disrupting control of vasodilation, tissue perfusion, hemostasis, and thrombosis. Nitric oxide bioavailability, crucial for maintaining vascular endothelial health and function, depends on the processes controlling synthesis and destruction of nitric oxide as well as on the sensitivity of target tissue to nitric oxide. Evidence supports a major contribution by oxidative stress-induced destruction of nitric oxide to the endothelial dysfunction that accompanies a number of cardiovascular disease states including hypertension, diabetes, chronic heart failure, and atherosclerosis. Regular physical activity (exercise training) reduces cardiovascular disease risk. Numerous studies support the hypothesis that exercise training improves vascular endothelial function, especially when it has been impaired by preexisting risk factors. Evidence is emerging to support a role for improved nitric oxide bioavailability with training as a result of enhanced synthesis and reduced oxidative stress-mediated destruction. Molecular targets sensitive to the exercise training effect include the endothelial nitric oxide synthase and the antioxidant enzyme superoxide dismutase. However, many fundamental details of the cellular and molecular mechanisms linking exercise to altered molecular and functional endothelial phenotypes have yet to be discovered. The working hypothesis is that some of the cellular mechanisms contributing to endothelial dysfunction in cardiovascular disease can be targeted and reversed by signals associated with regular increases in physical activity. The capacity for exercise training to regulate vascular endothelial function, nitric oxide bioavailability, and oxidative stress is an example of how lifestyle can complement medicine and pharmacology in the prevention and management of cardiovascular disease. Key words: exercise, artery, reactive oxygen species, antioxidant, hypertension


2014 ◽  
Vol 116 (2) ◽  
pp. 156-163 ◽  
Author(s):  
Rachelle E. Kaplon ◽  
Lindsey B. Gano ◽  
Douglas R. Seals

We tested the hypothesis that vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults. In 127 men and women aged 48–77 yr, brachial artery flow-mediated dilation (FMD) was positively related to dietary niacin intake [%change (Δ): r = 0.20, P < 0.05; mmΔ: r = 0.25, P < 0.01]. In subjects with above-average dietary niacin intake (≥22 mg/day, NHANES III), FMD was 25% greater than in subjects with below-average intake ( P < 0.05). Stepwise linear regression revealed that dietary niacin intake (above vs. below average) was an independent predictor of FMD (%Δ: β = 1.8; mmΔ: β = 0.05, both P < 0.05). Plasma oxidized low-density lipoprotein, a marker of systemic oxidative stress, was inversely related to niacin intake ( r = −0.23, P < 0.05) and was lower in subjects with above- vs. below-average niacin intake (48 ± 2 vs. 57 ± 2 mg/dl, P < 0.01). Intravenous infusion of the antioxidant vitamin C improved brachial FMD in subjects with below-average niacin intake ( P < 0.001, n = 33), but not above-average ( P > 0.05, n = 20). In endothelial cells sampled from the brachial artery of a subgroup, dietary niacin intake was inversely related to nitrotyrosine, a marker of peroxynitrite-mediated oxidative damage ( r = −0.30, P < 0.05, n = 55), and expression of the prooxidant enzyme, NADPH oxidase ( r = −0.44, P < 0.01, n = 37), and these markers were lower in subjects with above- vs. below-average niacin intake [nitrotyrosine: 0.39 ± 0.05 vs. 0.56 ± 0.07; NADPH oxidase: 0.38 ± 0.05 vs. 0.53 ± 0.05 (ratio to human umbilical vein endothelial cell control), both P < 0.05]. Our findings support the hypothesis that higher dietary niacin intake is associated with greater vascular endothelial function related to lower systemic and vascular oxidative stress among healthy middle-aged and older adults.


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