Abstract
Metabolic alterations such as insulin resistance are thought to underlie the endothelial dysfunction and low grade inflammation found in morbid obesity. Twenty-six morbidly obese patients, aged 39.0 +/- 10.0 (mean +/- sd), were evaluated before and 4.2 +/- 0.8 months after bariatric surgery. A marked increment in the insulin sensitivity index (S(I)) and the endothelium-dependent vasodilatory response in a dorsal hand vein was observed after weight loss following bariatric surgery. Circulating levels of E-selectin, P-selectin, plasminogen activator inhibitor-1, and von Willebrand factor, which were higher than those in the control group, decreased significantly after surgery. Plasma vascular cell adhesion molecule-1, angiotensin-converting enzyme, intercellular adhesion molecule-1, thrombomodulin, and plasma and intraplatelet cGMP levels did not change after weight loss. All inflammatory markers were higher in morbidly obese patients. After surgery, C- reactive protein and sialic acid diminished, whereas circulating levels of IL-6, TNF-alpha, and its soluble receptors did not. Positive correlations were found between changes in adiposity and S(I) and changes in C-reactive protein and between changes in sialic acid and changes in endothelial function. In conclusion, a marked improvement in S(I), endothelial function, and low grade inflammation was observed in the weight-losing, morbidly obese patients after bariatric surgery. S(I) and adiposity appear to play roles in obesity-related, low grade inflammation that contribute to the endothelial dysfunction observed in morbid obesity.
Highlights
Hyperinsulinemia and insulin resistance (IR) have been involved in vascular reactivity
In addition to reduction in IR, this marked weight loss has been found to be associated with improvement in the clustering of obesity-related metabolic
The present study demonstrated that in morbid obesity, venous vasodilatory function induced by Bk, an endotheliumdependent vasodilator [29], improved after bariatric surgery, and nitric oxide (NO) production and NO synthase activity are involved in the improvement in vascular reactivity
Summary
Hyperinsulinemia and IR have been involved in vascular reactivity. In the absence of IR, insulin has a direct vasodilatory effect [8, 9]. Increased serum levels of inflammatory biomarkers such as C-reactive protein (CRP) have been reported in obese subjects and have been related to the degree of insulin sensitivity and endothelial function [2, 3, 13]. PAI-1 levels, which were higher at baseline in obese patients, decreased after surgery to values similar to those in the control group.
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