Cho Young-Eun, Kim Hyung-Suk, Lai Chen, Stanfill Ansley, Cashion Ann
National Institute of Nursing Research, National Institutes of Health, 3 Center Drive, Building 3, Room 5E26, Bethesda, MD 20892-2178, USA.
University of Pittsburgh, 440 Victoria Building, 3500 Victoria St, Pittsburgh, PA 15261, USA.
Clin Biochem. 2016 Feb;49(3):237-42. doi: 10.1016/j.clinbiochem.2015.11.002. Epub 2015 Nov 9.
Weight gain after kidney transplantation (Tx) is considered a risk factor for poor outcomes. Increased oxidative stress is associated with not only chronic renal disease and Tx, but also obesity and cardiovascular disease. The aim of this pilot study was to test whether oxidative stress is related to weight gain at 12-months after kidney Tx and to obtain preliminary insight into potential mechanisms involved.
DESIGN & METHODS: Recipients (n=33) were classified into two groups; weight loss and weight gain, based on their weight changes at 12-months post-transplant. Total antioxidant capacity (TAOC) and lipid peroxidation (TBARS) were measured to evaluate oxidative stress from plasma at baseline and 12-months. A secondary data analysis was conducted to identify potential gene regulation.
Seventeen recipients lost (-6.63±5.52kg), and sixteen recipients gained weight (8.94±6.18kg). TAOC was significantly decreased at 12-months compared to baseline for the total group, however, there was no significant difference between groups at either time point. TBARS was higher in weight gain group, at both time points, and it was significantly higher at 12-months (p=0.012). Gene expression profiling analysis showed that 7 transcripts annotated to reactive oxygen species related genes in adipose tissue were expressed significantly lower in weight gain group at baseline, which might be a negative feedback mechanism to reduce oxidative stress.
These results may indicate that elevated oxidative stress (TBARS) is associated with weight gain after kidney Tx and that incorporating early clinical prevention strategies known to decrease oxidative stress could be recommended.
肾移植术后体重增加被认为是预后不良的一个危险因素。氧化应激增加不仅与慢性肾病和肾移植有关,还与肥胖和心血管疾病相关。本初步研究的目的是测试氧化应激是否与肾移植术后12个月时的体重增加有关,并初步了解其中潜在的机制。
根据肾移植术后12个月时的体重变化,将33名受者分为两组:体重减轻组和体重增加组。测量总抗氧化能力(TAOC)和脂质过氧化(TBARS),以评估基线和12个月时血浆中的氧化应激。进行二次数据分析以确定潜在的基因调控。
17名受者体重减轻(-6.63±5.52kg),16名受者体重增加(8.94±6.18kg)。与基线相比,全组在12个月时TAOC显著降低,但两组在任何一个时间点均无显著差异。体重增加组在两个时间点的TBARS均较高,且在12个月时显著更高(p=0.012)。基因表达谱分析显示,在脂肪组织中注释为与活性氧相关基因的7个转录本在体重增加组基线时表达显著较低,这可能是一种减少氧化应激的负反馈机制。
这些结果可能表明,氧化应激(TBARS)升高与肾移植术后体重增加有关,建议采用已知可降低氧化应激的早期临床预防策略。