Service of Endocrinology and Nutrition, University Hospital Doctor Peset-FISABIO, Av. Gaspar Aguilar 90, 46017, Valencia, Spain.
Service of Stomatology, University Hospital Doctor Peset-FISABIO, Av. Gaspar Aguilar 90, 46017, Valencia, Spain.
Int J Obes (Lond). 2019 Nov;43(11):2200-2209. doi: 10.1038/s41366-018-0309-5. Epub 2019 Jan 8.
The relationship between caloric restriction-mediated weight loss and the generation of ROS and its effects on atherosclerotic markers in obesity is not fully understood. Therefore, we set out to investigate whether dietary weight loss intervention improves markers of oxidative stress in leukocytes and subclinical parameters of atherosclerosis.
This was an interventional study of 59 obese subjects (BMI > 35 kg/m) who underwent 6 months of dietary therapy, including a 6-week very-low-calorie diet (VLCD) followed by an 18-week low-calorie diet (LCD). We determined clinical parameters, inflammatory markers-hsCRP, TNFα and NFκB -, oxidative stress parameters-total superoxide, glutathione, catalase activity and protein carbonyl groups-, soluble cellular adhesion molecules-sICAM, sP-selectin, sPSGL-1 -, myeloperoxidase (MPO), leukocyte-endothelium cell interactions-rolling flux, velocity and adhesion-and LDL subfractions, before and after the dietary intervention.
After losing weight, an improvement was observed in the patients' anthropometric, blood pressure and metabolic parameters, and was associated with reduced inflammatory response (hsCRP, TNFα and NFκB). Oxidative stress parameters improved, since superoxide production and protein carbonyl content were reduced and antioxidant systems were enhanced. In addition, a significant reduction of subclinical markers of atherosclerosis-small and dense LDL particles, MPO, sP-selectin and leukocyte adhesion-and an increase in soluble PSGL-1 were reported.
Our findings reveal that the improvement of subclinical atherosclerotic markers after dietary weight loss intervention is associated with a reduction of oxidative stress in leukocytes and inflammatory pathways, suggesting that these are the underlying mechanisms responsible for the reduced risk of cardiovascular disease in obese subjects after losing weight.
热量限制介导的体重减轻与 ROS 的产生及其对肥胖患者动脉粥样硬化标志物的影响之间的关系尚未完全阐明。因此,我们着手研究饮食减肥干预是否能改善白细胞氧化应激标志物和亚临床动脉粥样硬化参数。
这是一项对 59 名肥胖受试者(BMI>35kg/m²)进行的干预性研究,这些受试者接受了 6 个月的饮食治疗,包括 6 周的极低热量饮食(VLCD)和 18 周的低热量饮食(LCD)。我们测定了临床参数、炎症标志物-高敏 C 反应蛋白(hsCRP)、肿瘤坏死因子-α(TNFα)和核因子-κB(NFκB)-、氧化应激参数-总超氧化物、谷胱甘肽、过氧化氢酶活性和蛋白羰基组-、可溶性细胞间黏附分子-sICAM、sP-选择素、sPSGL-1-、髓过氧化物酶(MPO)、白细胞-内皮细胞相互作用-滚动流、速度和黏附-和 LDL 亚组分,在饮食干预前后进行测定。
减肥后,患者的人体测量学、血压和代谢参数得到改善,与炎症反应降低(hsCRP、TNFα 和 NFκB)有关。氧化应激参数得到改善,因为超氧化物的产生和蛋白羰基含量减少,抗氧化系统增强。此外,亚临床动脉粥样硬化标志物(小而密的 LDL 颗粒、MPO、sP-选择素和白细胞黏附)显著减少,可溶性 PSGL-1 增加。
我们的研究结果表明,饮食减肥干预后亚临床动脉粥样硬化标志物的改善与白细胞氧化应激和炎症途径的减少有关,这表明这些是肥胖患者减肥后心血管疾病风险降低的潜在机制。