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The loss of endothelial function is one of the most commonly observed vascular effects of mercury exposure [ 5– 9].
However, the fact that eNOS is preferentially ubiquitinated suggests that the loss of endothelial function during hyperglycemia associated with a loss of eNOS activity may be due to a combination of excessive oxidative stress and UPS-dependent proteolysis [ 46].
While there is a loss in nitric oxide production with age, it is not clear if this is the sole culprit in causing a loss of endothelial function with age.
The loss of endothelial function in sepsis is known to promote impaired local regulation of vascular responsiveness; impaired vascular autoregulation, tissue metabolism/perfusion mismatch, increased intravascular coagulation, and platelet/neutrophil adhesion/activation [ 8, 20– 20].
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Effects of weight loss on endothelial function are however not clear.
Also, circulating TNF-α levels are associated with impaired skin capillary recruitment (44), and weight loss resulted in a significant amelioration of endothelial function that closely correlated with a reduction in circulating TNF-α (32).
Consistently, we observed NO loss-related endothelial dysfunction and protection of endothelial function provided by eNOS enhancement in porcine coronary arteries which underwent 1 h of hypoxic exposure in St. Thomas cardioplegic (ST) solution and 30 min reoxygenation [ 26].
The hypothesis that microvascular dysfunction may precede and predict the development of insulin resistance and hypertension is supported by the presence of microvascular dysfunction in normoglycemic mildly overweight individuals with a genetic predisposition for type 2 diabetes (31) and improvement of endothelial function by weight loss in obese women (32).
These prior findings indicate that Caveolin-1 plays an important role in the regulation of endothelial function and that the loss of Caveolin-1 in BVECs induces BBB hyperpermeability.
This is in accord with other studies showing that changes in clinical and serum markers of endothelial function in response to moderate weight loss do not always correlate.
Therefore, we performed a meta-analysis to quantify effects of weight loss on flow-mediated vasodilation (FMD) of the brachial artery, a measurement of endothelial function.
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