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代谢综合征患者血清细胞黏附分子与 hs-CRP 、尿酸及 VEGF 基因多态性的相关性
Metabolic syndrome (MetS) is associated with a pro-inflammatory state and endothelial dysfunction that places subjects with MetS at a higher risk of atherosclerosis. Inflammatory biomarkers are raised in patients at risk of developing cardiovascular diseases. In the current study, we aimed to examine the possible association between MetS and serum soluble adhesion molecules, hs-CRP, uric acid, and the genetic variations related to vascular endothelial growth factor (VEGF) gene. In this cross-sectional study, participants were enrolled from the Mashhad stroke and heart atherosclerotic disorders (MASHAD) study. The International Diabetes Federation criteria were used to define the MetS. Cell adhesion molecules (CAM) and serum hs-CRP were measured by ELISA and PEG-enhanced immunoturbidimetry method, respectively. We used a logistic regression analysis to determine independent associations of CAMs with the VEGF polymorphisms and MetS. Two hundred and 59 participants with and without MetS were enrolled. Participants with MetS and DM had a significantly higher serum E-selectin level (p < 0.05). Participants with a high serum E-selectin level had higher levels of hs-CRP, FBG, TG, uric acid, BMI and lower levels of serum HDL-C (p < 0.05). Interestingly, individuals with MetS with a genetic variant of the VEGF gene (rs6921438) had higher level of serum ICAM-1 (p = 0.04). There were significant associations between serum E-selectin concentrations and the presence of MetS, and its risk factors. Moreover, we demonstrated that MetS subjects with the rs6921438 genetic variant had a higher serum level of ICAM-1 (p < 0.05).
代谢综合征 (MetS) 与促炎症状态和内皮功能障碍相关,使 MetS 受试者发生动脉粥样硬化的风险更高。有发生心血管疾病风险的患者炎症生物标志物升高。在目前的研究中,我们旨在研究 MetS 与血清可溶性黏附分子、 hs-CRP 、尿酸以及与血管内皮生长因子 (VEGF) 相关的遗传变异之间的可能关联吉恩。在这项横断面研究中,参与者来自马什哈德卒中和心脏动脉粥样硬化疾病 (MASHAD) 研究。使用国际糖尿病联盟标准定义 MetS。分别采用 ELISA 法和 PEG 增强免疫比浊法测定细胞黏附分子 (CAM) 和血清 hs-CRP。我们采用 logistic 回归分析确定 CAMs 与 VEGF 多态性和 MetS 的独立相关性。入选了两百五十九例伴或不伴 MetS 的参与者。MetS 和 DM 患者血清 E-选择素水平显著升高 (p
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METHODS:BACKGROUND:Given the importance of habitual dietary protein intake, distribution patterns and dietary sources in the aetiology of age-related declines of muscle mass and function, the present study examined these factors as a function of sex and age in Irish adults aged 18-90 years comprising The National Adult Nutrition Survey (NANS). METHODS:In total, 1051 (males, n = 523; females, n = 528) undertook a 4-day semi-weighed food diary. Total, body mass relative intake and percentage contribution to total energy intake of dietary protein were determined in addition to protein distribution scores (PDS), as well as the contribution of food groups, animal- and plant-based foods to total protein intake. RESULTS:Total and relative protein intake [mean (SD)] were highest in those aged 18-35 years [96 (3) g day , 1.32 (0.40) g kg day ], with lower protein intakes with increasing age (i.e. in adults aged ≥65 years [82 (22) g, 1.15 (0.34) g kg day , P < 0.001 for both]. Differences in protein intake between age groups were more pronounced in males compared to females. Protein distribution followed a skewed pattern for all age groups [breakfast, 15 (10) g; lunch, 30 (15) g; dinner, 44 (17) g]. Animal-based foods were the dominant protein source within the diet [63% (11%) versus 37% (11%) plant protein, P < 0.001]. CONCLUSIONS:Protein intake and the number of meals reaching the purported threshold for maximising post-prandial anabolism were highest in young adults, and lower with increasing age. For main meals, breakfast provided the lowest quantity of protein across all age categories and may represent an opportunity for improving protein distribution, whereas, in older adults, increasing the number of meals reaching the anabolic threshold regardless of distribution pattern may be more appropriate.
METHODS:BACKGROUND:Low cardiorespiratory fitness (CRF) increases risk of all-cause mortality and cardiovascular events. Periodic CRF assessment can have an important preventive function. OBJECTIVE:To develop a protocol-free method to estimate CRF in daily life based on heart rate (HR) and body acceleration measurements. METHODS:Acceleration and HR data were collected from 37 subjects (M=49%) while performing a standardized laboratory activity protocol (sitting, walking, running, cycling) and during a 5-days free-living monitoring period. CRF was determined by oxygen uptake (VO2max) during maximal exercise testing. A doubly-labeled water validated equation was used to predict total energy expenditure (TEE) from acceleration data. A fitness index was defined as the ratio between TEE and HR (TEE-pulse). Activity recognition techniques were used to process acceleration features and classify sedentary, ambulatory and other activity types. Regression equations based on TEE-pulse data from each activity type were developed to predict VO2max. RESULTS:TEE-pulse measured within each activity type of the laboratory protocol was highly correlated to VO2max (r from 0.74 to 0.91). Averaging the outcome of each activity-type specific equation based on TEE-pulse from the laboratory data led to accurate estimates of VO2max (RMSE: 300.0 mlO2/min or 10%). The difference between laboratory and free-living determined TEE-pulse was 3.7 ± 11% (r =0.85). The prediction method preserved the prediction accuracy when applied to free-living data (RMSE: 367 mlO2/min or 12%). CONCLUSIONS:Measurements of body acceleration and HR can be used to predict VO2max in daily life. Activity-specific prediction equations are needed to achieve highly accurate estimates of CRF.
METHODS:OBJECTIVE:Postprandial dyslipidemia is a common feature of insulin resistant states and contributes to increased cardiovascular disease risk. Recently, bile acids have been recognized beyond their emulsification properties as important signaling molecules that promote energy expenditure, improve insulin sensitivity, and lower fasting lipemia. While bile acid receptors have become novel pharmaceutical targets, their effects on postprandial lipid metabolism remain unclear. Here we investigated the potential role of bile acids in regulation of postprandial chylomicron production and triglyceride excursion. Approach and Results: Healthy C57BL/6 mice were given an intraduodenal infusion of taurocholic acid (TA) under fat-loaded conditions and circulating lipids were measured. Targeting of bile acid receptors was achieved with GW4064, a synthetic agonist to the farnesoid X receptor (FXR), and with deoxycholic acid (DCA), an activator of the Takeda G-protein-coupled receptor 5. TA, GW4064, and DCA treatments all lowered postprandial lipemia. FXR agonism also reduced intestinal triglyceride content and activity of microsomal triglyceride transfer protein, involved in chylomicron assembly. Importantly, TA effects (but not DCA) were largely lost in FXR knockout mice. These bile acid effects are reminiscent of the anti-diabetic hormone glucagon-like peptide-1 (GLP-1). While the GLP-1 receptor agonist exendin-4 retained its ability to acutely lower postprandial lipemia during bile acid sequestration and FXR deficiency, it did raise hepatic expression of the rate limiting enzyme for bile acid synthesis. CONCLUSIONS:Bile acid signaling may be an important mechanism of controlling dietary lipid absorption and bile acid receptors may constitute novel targets for the treatment of postprandial dyslipidemia.