Department of Pathology and Laboratory Medicine, University of California at Davis, Medical Center, 4635 Second Avenue, Research 1 Building, Room 3000, Sacramento, California 95817, USA.
J Clin Endocrinol Metab. 2012 Oct;97(10):E1844-50. doi: 10.1210/jc.2012-2498. Epub 2012 Aug 7.
Metabolic syndrome (MetS) confers a greater risk for both cardiovascular disease (CVD) and diabetes. Oxidative stress (OS) could contribute to this excess risk. However, there are few data examining both cellular and circulating biomarkers of OS in MetS uncomplicated by diabetes and CVD.
The aim of the study was to evaluate both cellular and circulating biomarkers of OS in MetS uncomplicated by diabetes or CVD.
At an academic medical center, we compared MetS (n=43) vs. control subjects (n=33). Fasting blood was collected for monocyte isolation and assay of OS biomarkers.
Monocyte nicotinamide adenine dinucleotide phosphate oxidase activity (p22 phox and p47), superoxide anion release, oxidized-low-density lipoprotein (Ox-LDL), nitrotyrosine, and nuclear factor erythroid 2-related factor were measured.
There was significantly increased release of superoxide from the monocytes (basal and after activation) of MetS compared with controls adjusted for body mass index. Body mass index-adjusted plasma levels of Ox-LDL and nitrotyrosine were significantly increased in MetS. There was a linear trend between biomarkers of oxidative stress and increasing number of features of MetS. Also, there was a significant increase in nicotinamide adenine dinucleotide phosphate oxidase membrane expression of p22 phox and p47 phox in MetS. The major cellular antioxidant defense, nuclear factor erythroid 2-related factor was significantly decreased. There were significant correlations between homeostasis model assessment insulin resistance index and both Ox-LDL and nitrotyrosine and superoxide and Ox-LDL.
Collectively, nascent MetS is associated with increased OS as evidenced by both circulating and cellular biomarkers, and this could contribute to the risk for both diabetes and CVD.
代谢综合征（MetS）会增加心血管疾病（CVD）和糖尿病的风险。氧化应激（OS）可能导致这种风险增加。然而，目前很少有数据研究未经糖尿病和 CVD 合并的 MetS 患者细胞和循环 OS 生物标志物。
本研究旨在评估未经糖尿病或 CVD 合并的 MetS 患者的细胞和循环 OS 生物标志物。
在一所学术医疗中心，我们比较了 MetS（n=43）和对照组（n=33）。采集空腹血用于分离单核细胞并检测 OS 生物标志物。
测量了单核细胞烟酰胺腺嘌呤二核苷酸磷酸氧化酶活性（p22 phox 和 p47）、超氧阴离子释放、氧化型低密度脂蛋白（Ox-LDL）、硝基酪氨酸和核因子红细胞 2 相关因子。
与对照组相比，MetS 患者的单核细胞（基础和激活后）超氧阴离子释放明显增加，调整了体重指数。MetS 患者的血浆 Ox-LDL 和硝基酪氨酸水平明显升高。氧化应激生物标志物与 MetS 特征的增加呈线性趋势。此外，MetS 患者烟酰胺腺嘌呤二核苷酸磷酸氧化酶膜表达 p22 phox 和 p47 phox 显著增加。主要的细胞抗氧化防御物核因子红细胞 2 相关因子显著减少。稳态模型评估的胰岛素抵抗指数与 Ox-LDL 和硝基酪氨酸以及超氧阴离子和 Ox-LDL 均呈显著相关性。
总的来说，新生的 MetS 与循环和细胞生物标志物均表明 OS 增加，这可能导致糖尿病和 CVD 的风险增加。
