Department of Biochemistry and Molecular Biology (BK21 Project), Medical Research Center for Bioreaction to Reactive Oxygen Species, School of Medicine, Kyung Hee University, No. 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, South Korea.
Br J Nutr. 2011 Nov;106(10):1544-51. doi: 10.1017/S0007114511002091. Epub 2011 Jun 8.
It has been reported that high-fat, high-carbohydrate (HFHC) meals increase oxidative stress and inflammation. We examined whether repeated intake of excess energy in the form of HFHC meals alters reactive oxygen species (ROS) generation and the expression levels of antioxidant enzymes and mitochondrial proteins in mononuclear cells, and to determine whether this is associated with insulin resistance. We recruited healthy lean individuals (n 10). The individuals were divided into two groups: one group (n 5) ingested 10878·4 kJ/d (2600 kcal/d; 55-70 % carbohydrate, 9·5-16 % fat, 7-20 % protein) recommended by the Dietary Reference Intake for Koreans for 4 d and the other group (n 5) ingested a HFHC meal containing 14 644 kJ/d (3500 kcal/d). Then, measurements of blood insulin and glucose levels, together with suppressor of cytokine signalling-3 (SOCS-3) expression levels, were performed in both groups. Also, cellular and mitochondrial ROS levels as well as malondialdehyde (MDA) levels were measured. Expression levels of cytosolic and mitochondrial antioxidant enzymes, and mitochondrial complex proteins were analysed. Repeated intake of HFHC meals induced an increase in homeostasis model of assessment-insulin resistance (HOMA-IR), together with an increase in SOCS-3 expression levels. While a single intake of the HFHC meal increased cytosolic and mitochondrial ROS, repeated intake of HFHC meals reduced them and increased the levels of MDA, cytosolic and mitochondrial antioxidant enzymes, and several mitochondrial complex proteins. Repeated intake of HFHC meals induced cellular antioxidant mechanisms, which in turn increased lipid peroxidation (MDA) and SOCS-3 expression levels, induced hyperinsulinaemia and increased HOMA-IR, an index of insulin resistance. In conclusion, excess energy added to a diet can generate detrimental effects in a short period.
据报道，高脂肪、高碳水化合物（HFHC）膳食会增加氧化应激和炎症。我们研究了反复摄入过量能量（以 HFHC 膳食形式）是否会改变单核细胞中活性氧（ROS）的产生和抗氧化酶及线粒体蛋白的表达水平，并确定这是否与胰岛素抵抗有关。我们招募了健康的瘦个体（n 10）。将这些个体分为两组：一组（n 5）摄入由韩国膳食参考摄入量推荐的 10878·4 kJ/d（2600 kcal/d；碳水化合物 55-70%、脂肪 9.5-16%、蛋白质 7-20%），持续 4 d；另一组（n 5）摄入含有 14644 kJ/d（3500 kcal/d）的 HFHC 膳食。然后，在两组中均进行了血液胰岛素和葡萄糖水平的测量，以及抑制细胞因子信号转导 3（SOCS-3）表达水平的测量。还测量了细胞和线粒体 ROS 水平以及丙二醛（MDA）水平。分析了胞质和线粒体抗氧化酶以及线粒体复合物蛋白的表达水平。重复摄入 HFHC 膳食会导致稳态模型评估-胰岛素抵抗（HOMA-IR）增加，同时 SOCS-3 表达水平增加。单次摄入 HFHC 膳食会增加胞质和线粒体 ROS，而重复摄入 HFHC 膳食会降低它们并增加 MDA、胞质和线粒体抗氧化酶以及几种线粒体复合物蛋白的水平。重复摄入 HFHC 膳食诱导细胞抗氧化机制，从而增加脂质过氧化（MDA）和 SOCS-3 表达水平，诱导高胰岛素血症和增加 HOMA-IR，这是胰岛素抵抗的一个指标。总之，饮食中添加过多的能量会在短时间内产生有害影响。
