Laboratory of Human Genetics, School of Food and Nutritional Sciences, Graduate School of Nutritional and Environmental Sciences, Global COE Program, University of Shizuoka, Shizuoka, Japan.
Obesity (Silver Spring). 2011 Apr;19(4):882-7. doi: 10.1038/oby.2010.275. Epub 2010 Dec 2.
Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the antioxidant capacity of the cell. This imbalance and an excess of ROS induce tissue/cellular damage, which are implicated in chronic inflammation disorders such as obesity, insulin resistance, and metabolic syndromes. Peroxiredoxins (Prxs) are the most abundant and ancient cellular antioxidant proteins that help to control intracellular peroxide levels and ROS-dependent signaling. Of the six mammalian isoforms, Prx III is specifically localized in mitochondria. In this study, we detected novel associations between genetic variations of the PRDX3 gene and BMI and obesity risk in the general Japanese population. In addition, these associations were observed only in the subjects with high dietary fat intake, but not in the subjects with low dietary fat intake. These findings indicate that the interaction between genetic variations in the PRDX3 gene and dietary fat intake is important for modulation of BMI and obesity risk.
氧化应激是由活性氧（ROS）的产生与细胞抗氧化能力之间的失衡引起的。这种失衡和 ROS 的过度产生会导致组织/细胞损伤，这与肥胖、胰岛素抵抗和代谢综合征等慢性炎症疾病有关。过氧化物酶（Prxs）是最丰富和古老的细胞抗氧化蛋白，有助于控制细胞内过氧化物水平和 ROS 依赖性信号转导。在六种哺乳动物同工酶中，Prx III 特异性定位于线粒体。在这项研究中，我们在普通日本人群中检测到 PRDX3 基因的遗传变异与 BMI 和肥胖风险之间的新关联。此外，这些关联仅在高膳食脂肪摄入的受试者中观察到，而在低膳食脂肪摄入的受试者中未观察到。这些发现表明，PRDX3 基因的遗传变异与膳食脂肪摄入之间的相互作用对于调节 BMI 和肥胖风险很重要。
