Abstract
Little is known about the mechanisms underlying the cardioprotective effect of Roux en-Y gastric bypass (RYGB) surgery. Therefore, the aim of the present study was to investigate whether weight loss associated with RYGB improves the oxidative status of leukocytes and ameliorates subclinical atherosclerotic markers. This is an interventional study of 57 obese subjects who underwent RYGB surgery. We determined biochemical parameters and qualitative analysis of cholesterol, leukocyte and systemic oxidative stress markers —superoxide production, glutathione peroxidase 1 (GPX1), superoxide dismutase (SOD) activity and protein carbonylation—, soluble cellular adhesion molecules —sICAM-1 and sP-selectin—, myeloperoxidase (MPO) and leukocyte-endothelium cell interactions—rolling flux, velocity and adhesion. RYGB induced an improvement in metabolic parameters, including hsCRP and leukocyte count (p < 0.001, for both). This was associated with an amelioration in oxidative stress, since superoxide production and protein carbonylation were reduced (p < 0.05 and p < 0.01, respectively) and antioxidant systems were enhanced (GPX1; p < 0.05 and SOD; p < 0.01). In addition, a significant reduction of the following parameters was observed one year after RYGB: MPO and sICAM (p < 0.05, for both), sPselectin and pattern B of LDL particles (p < 0.001, for both), and rolling flux and adhesion of leukocytes (p < 0.05 and p < 0.01, respectively). Our results suggest that patients undergoing RYGB benefit from an amelioration of the prooxidant status of leukocytes, metabolic outcomes, and subclinical markers of atherosclerosis.
Highlights
Obesity is an endocrine disease with an important inflammatory component [1] that underlies the development of clinical complications such as type 2 diabetes (T2D), arterial hypertension, dyslipidemia and metabolic syndrome, all of which are considered major risk factors for cardiovascular disease (CVD) [2]
Previous studies have reported an impairment of the main antioxidant systems in morbid obesity, including superoxide dismutase (SOD), catalase and glutathione peroxidase (GPX) [10,11], which are considered the front line of enzymatic reactive oxygen species (ROS) scavenging
There was a reduction in blood leukocyte count (p < 0.001) and a significant decrease in levels of the acute phase inflammation reactants high sensitivity C-reactive protein (hsCRP) and C3 fraction of the complement (C3c) (p < 0.001), suggesting an amelioration of the systemic inflammatory response
Summary
Obesity is an endocrine disease with an important inflammatory component [1] that underlies the development of clinical complications such as type 2 diabetes (T2D), arterial hypertension, dyslipidemia and metabolic syndrome, all of which are considered major risk factors for cardiovascular disease (CVD) [2]. Vascular health is impaired in several ways during obesity, including arterial stiffening, endothelial dysfunction and atherosclerosis, which are primary phases in the development of major cardiovascular complications including stroke and coronary diseases. In this context, proinflammatory status, insulin resistance (IR), and oxidative stress are recognized as major inducers of vascular damage and endothelial dysfunction [5,6,7]. Oxidative stress is a hallmark of obesity caused by undermined antioxidant capacity in conjunction with increased levels of reactive oxygen species (ROS) production. Previous studies have reported an impairment of the main antioxidant systems in morbid obesity, including superoxide dismutase (SOD), catalase and glutathione peroxidase (GPX) [10,11], which are considered the front line of enzymatic ROS scavenging
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
