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Bariatric surgery reduces CD36-bearing microvesicles of endothelial and monocyte origin

机译:牛肝外科减少了内皮和单核细胞起源的CD36微铅

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摘要

Abstract Background Bariatric surgery is a widely adopted treatment for obesity and its secondary complications. In the past decade, microvesicles (MVs) and CD36 have increasingly been considered as possible biomarkers for obesity, the metabolic syndrome (MetSy), type 2 diabetes mellitus (T2DM). Thus, the purpose of this study was to investigate how weight loss resulting from bariatric surgery affects levels of specific MV phenotypes and their expression of CD36 scavenger receptor. Additionally, we hypothesised that subjects with MetSy had higher baseline concentrations of investigated MV phenotypes. Methods Twenty individuals undergoing Roux-en-Y gastric bypass surgery were evaluated before and 3 months after surgery. MVs were characterised by flow cytometry at both time points and defined as lactadherin-binding particles within a 100-1000 nm size gate. MVs of monocyte (CD14) and endothelial (CD62E) origin were defined by cell-specific markers, and their expression of CD36 was investigated. Results Following bariatric surgery, subjects incurred an average BMI reduction (delta) of − 8.4 ± 1.4 (p < 0.0001). Significant reductions were observed for the total MVs (− 66.55%, p = 0.0017) and MVs of monocyte (− 36.11%, p = 0.0056) and endothelial (− 40.10%, p = 0.0007) origins. Although the bulk of CD36-bearing MVs were unaltered, significant reductions were observed for CD36-bearing MVs of monocyte (− 60.04%, p = 0.0192) and endothelial (− 54.93%, p = 0.04) origin. No differences in levels of MVs were identified between subjects who presented with MetSy at baseline (n = 13) and those that did not (n = 7). Conclusion Bariatric surgery resulted in significantly altered levels of CD36-bearing MVs of monocyte and endothelial origin. This likely reflects improvements in ectopic fat distribution, plasma lipid profile, low-grade inflammation, and oxidative stress following weight loss. Conversely, however, the presence of MetSy at baseline had no impact on MV phenotypes.
机译:摘要背景减肥手术是对肥胖及其并发症继发广泛采用的治疗方法。在过去的十年中,微泡(MVS)和CD36越来越多地被视为肥胖可能的生物标记物,代谢综合征(MetSy),2型糖尿病(T2DM)。因此,本研究的目的是调查的减肥手术导致体重下降如何影响特定的MV表型的水平和他们CD36清道夫受体的表达。此外,我们假设,与MetSy受试者调查MV表型的较高的基线浓度。方法二个人经历空肠Roux-en-Y胃旁路手术前进行评估,手术后3个月。的MV在两个时间点进行表征通过流式细胞术和定义为100-1000纳米的尺寸内浇口乳凝集素结合颗粒。单核细胞的的MV(CD14)和内皮(CD62E)原点通过细胞特异性标记物所定义,并研究了它们的CD36的表达。结果如下减肥手术,受试者发生的平均BMI减少(△) - 8.4±1.4(P <0.0001)。观察到总的MV显著减量( - 66.55%,P = 0.0017)和单核细胞的的MV( - 36.11%,P = 0.0056)和内皮( - 40.10%,p值= 0.0007)的起源。虽然CD36-轴承MV的大部分是未改变的,观察到单核细胞的CD36-轴承的MV显著减量( - 60.04%,P = 0.0192)和内皮( - 54.93%,p值= 0.04)的起源。在MV的水平没有差异,确定谁在基线(N = 13)MetSy呈现主题和那些没有(N = 7)之间。结论减肥手术导致单核细胞和内皮来源的CD36轴承的MV显著水平改变。这可能反映在以下减肥异位脂肪分布,血脂谱,低度炎症和氧化应激的改进。但是,相反,MetSy的基线存在对MV的表型没有影响。

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