Effects of lifestyle modification on central artery stiffness in metabolic syndrome subjects with pre-hypertension and/or pre-diabetes

Aizawa, Kunihiko; Shoemaker, J. Kevin; Overend, Tom J.; Petrella, Robert J.

doi:10.1016/j.diabres.2008.11.016

Cited by 42 publications

(46 citation statements)

References 23 publications

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“…18 Improved vascular function may be the mechanism responsible for the reduction in BP. Aizawa and colleagues 24 found a significant increase in distensibility in patients with MS following 8 weeks of physician-prescribed exercise and Mediterranean diet.…”

Section: Discussionmentioning

confidence: 99%

Diabetes and Technology for Increased Activity (DaTA) Study: Results of a Remote Monitoring Intervention for Prevention of Metabolic Syndrome

Stuckey

Russell-Minda

Read

et al. 2011

J Diabetes Sci Technol

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Section: Discussionmentioning

confidence: 99%

Diabetes and Technology for Increased Activity (DaTA) Study: Results of a Remote Monitoring Intervention for Prevention of Metabolic Syndrome

Stuckey

Russell-Minda

Read

et al. 2011

J Diabetes Sci Technol

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“…In humans, aerobic exercise has been shown to decrease arterial stiffness and increases endothelial-mediated vasodilatation in people with diabetes (2,26,24). Studies by YoungLee and colleagues in mouse skeletal muscle revealed decreased exercise capacity in eNOS Ϫ/Ϫ mice, coincident with impaired signaling through AMPK in response to exercise (22).…”

Section: ·Daymentioning

confidence: 99%

Nitric oxide regulates vascular adaptive mitochondrial dynamics

Miller

Knaub

Olivera-Fragoso

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Miller MW, Knaub LA, Olivera-Fragoso LF, Keller AC, Balasubramaniam V, Watson PA, Reusch JE. Nitric oxide regulates vascular adaptive mitochondrial dynamics. Am J Physiol Heart Circ Physiol 304: H1624 -H1633, 2013. First published April 12, 2013 doi:10.1152/ajpheart.00987.2012.-Cardiovascular disease risk factors, such as diabetes, hypertension, dyslipidemia, obesity, and physical inactivity, are all correlated with impaired endothelial nitric oxide synthase (eNOS) function and decreased nitric oxide (NO) production. NO-mediated regulation of mitochondrial biogenesis has been established in many tissues, yet the role of eNOS in vascular mitochondrial biogenesis and dynamics is unclear. We hypothesized that genetic eNOS deletion and 3-day nitric oxide synthase (NOS) inhibition in rodents would result in impaired mitochondrial biogenesis and defunct fission/fusion and autophagy profiles within the aorta. We observed a significant, eNOS expression-dependent decrease in mitochondrial electron transport chain (ETC) protein subunits from complexes I, II, III, and V in eNOS heterozygotes and eNOS null mice compared with age-matched controls. In response to NOS inhibition with N G -nitro-L-arginine methyl ester (L-NAME) treatment in Sprague Dawley rats, significant decreases were observed in ETC protein subunits from complexes I, III, and IV as well as voltagedependent anion channel 1. Decreased protein content of upstream regulators of mitochondrial biogenesis, cAMP response elementbinding protein and peroxisome proliferator-activated receptor-␥ coactivator-1␣, were observed in response to 3-day L-NAME treatment. Both genetic eNOS deletion and NOS inhibition resulted in decreased manganese superoxide dismutase protein. L-NAME treatment resulted in significant changes to mitochondrial dynamic protein profiles with decreased fusion, increased fission, and minimally perturbed autophagy. In addition, L-NAME treatment blocked mitochondrial adaptation to an exercise intervention in the aorta. These results suggest that eNOS/NO play a role in basal and adaptive mitochondrial biogenesis in the vasculature and regulation of mitochondrial turnover.endothelial nitric oxide synthase; vascular mitochondria THE VASCULATURE IS A COMPLEX tissue with a cellular architecture that permits specific contractile profiles for optimal tissue perfusion and adaptation to physiological demands. One of the primary regulators of physiological vasomotion is nitric oxide (NO), generated enzymatically by a family of nitric oxide synthases (NOS): endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS. In addition to the regulation of blood flow, NO modulates vascular structure and function through direct signaling to vascular endothelium, vascular smooth muscle cells, and inflammatory and adventitial cells (reviewed in Ref. 11). Endothelium-derived NO is a physiologically significant vasodilator and inhibitor of platelet aggregation and adhesion. Vascular NO also prevents leukocyte adhesion to the endothelium and inhibits proliferation of vas...

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“…Lifestyle modifications (lowfat, low-sodium diet and regular exercise) leading to weight loss decreases arterial stiffness in patients with obesity and the metabolic syndrome. 60,61 Similarly, 4 weeks of supervised aerobic exercise led to significant decreases in central (aortic) PWV and peripheral (femoral-dorsalis pedis) PWV (arterial 'de-stiffening') in hypertensive patients. 62 Such results were not reproduced with resistance training, which in fact increased both central PWV and peripheral PWV.…”

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confidence: 99%

Arterial dysfunction and functional performance in patients with peripheral artery disease: A review

2011

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Functional performance influences quality of life in individuals with peripheral artery disease (PAD) and is also a powerful prognostic marker in these patients. The pathophysiology of impaired functional performance in patients with PAD is incompletely understood. The severity of atherosclerotic burden, non-invasively assessed by the ankle-brachial index (ABI), does not reliably predict the degree of functional impairment observed in PAD patients. We review associations of measures of arterial function (arterial stiffness and endothelial dysfunction) with functional performance in PAD patients, and also review potential therapies for arterial stiffness and endothelial dysfunction that could improve functional performance in PAD. Recent studies suggest that measures of arterial function, such as arterial stiffness and endothelial function, are associated with exercise performance in the setting of PAD. These studies have provided new insights into (1) the pathophysiology of functional impairment in PAD, (2) mechanisms of strategies known to be effective such as walking programs, and (3) potential new therapeutic interventions for improving functional performance. Thus, therapies aimed at arterial 'de-stiffening' and improving endothelial function (such as aerobic exercise, statins and angiotensinconverting enzyme inhibitors) may improve functional performance in patients with PAD; however, further investigations are needed.

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Effects of lifestyle modification on central artery stiffness in metabolic syndrome subjects with pre-hypertension and/or pre-diabetes

Cited by 42 publications

References 23 publications

Diabetes and Technology for Increased Activity (DaTA) Study: Results of a Remote Monitoring Intervention for Prevention of Metabolic Syndrome

Diabetes and Technology for Increased Activity (DaTA) Study: Results of a Remote Monitoring Intervention for Prevention of Metabolic Syndrome

Nitric oxide regulates vascular adaptive mitochondrial dynamics

Arterial dysfunction and functional performance in patients with peripheral artery disease: A review

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