Crujeiras Ana B, Parra Dolores, Goyenechea Estíbaliz, Abete Itziar, Martínez J Alfredo
Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, Pamplona, Spain.
Eur J Nutr. 2009 Sep;48(6):341-7. doi: 10.1007/s00394-009-0019-9. Epub 2009 Apr 10.
Postprandially induced oxidative stress can cause damage to mitochondrial components and initiate cellular degradative processes; which are related to obesity comorbidities.
This trial sought to determine whether weight loss induced by caloric restriction provides antioxidant protection to reduce the postprandial response of mitochondrial function and oxidative stress markers.
A group of overweight/obese volunteers (n = 17; 39 +/-7 years, 32.5 +/- 4.8 kg/m(2)) followed an 8-week hypocaloric diet. Volunteers provided blood samples at fasting and 2-h after a test drink (CHO: 95% E, PROT: 5% E and containing antioxidants) and these were examined for postprandial oxidative stress responses, before and after the nutritional intervention. The expression of four mitochondrial-related genes, COX15, NDUFS2, MGST2 and TNF-alfa, was measured in peripheral blood mononuclear cells (PBMC) by quantitative RT-PCR. Lipid peroxidation and nitrosative stress biomarkers, total antioxidant capacity (AOP), uric acid and glutathione peroxidase were also determined.
Before nutritional treatment, the test drink induced a postprandial increase in lipid peroxidation and nitrosative stress biomarkers with a concomitant increase in the AOP. The increase in postprandial oxidative stress biomarkers was accompanied by a decrease in PBMC COX15 mRNA levels. Interestingly, after the weight loss period (-5.8 +/- 2.3%), the postprandial-induced changes were lower than at the beginning of the study and involved oxidative stress biomarkers and the COX15 and MGST2 transcripts. This finding suggests the occurrence of a tachyphylactic process.
We demonstrate for the first time that the well-known effect of energy restriction on oxidative stress is accompanied by a tolerance mechanism on the postprandial oxidative stress response and mitochondrial function-related genes. Indeed, the COX15 and MGST2 gene expression assays in PBMC emerged as valuable nutrigenomic biomarkers of the oxidative response under energy-restriction conditions.
餐后诱导的氧化应激可导致线粒体成分受损并引发细胞降解过程，这与肥胖合并症相关。
本试验旨在确定热量限制引起的体重减轻是否能提供抗氧化保护，以降低线粒体功能和氧化应激标志物的餐后反应。
一组超重/肥胖志愿者（n = 17；39±7岁，32.5±4.8 kg/m²）遵循8周的低热量饮食。志愿者在空腹时以及饮用测试饮料（碳水化合物：95%能量，蛋白质：5%能量且含有抗氧化剂）后2小时提供血样，并在营养干预前后检测这些血样的餐后氧化应激反应。通过定量逆转录聚合酶链反应在外周血单核细胞（PBMC）中测量四个线粒体相关基因COX15、NDUFS2、MGST2和TNF-α的表达。还测定了脂质过氧化和亚硝化应激生物标志物、总抗氧化能力（AOP）、尿酸和谷胱甘肽过氧化物酶。
在营养治疗前，测试饮料诱导餐后脂质过氧化和亚硝化应激生物标志物增加，同时AOP增加。餐后氧化应激生物标志物的增加伴随着PBMC中COX15 mRNA水平的降低。有趣的是，在体重减轻期（-5.8±2.3%）后，餐后诱导的变化低于研究开始时，涉及氧化应激生物标志物以及COX15和MGST2转录本。这一发现表明发生了快速耐受过程。
我们首次证明，能量限制对氧化应激的众所周知的影响伴随着对餐后氧化应激反应和线粒体功能相关基因的耐受机制。事实上，PBMC中COX15和MGST2基因表达测定成为能量限制条件下氧化反应的有价值的营养基因组生物标志物。
