Inflammatory bowel disease (IBD) is often associated with a decrease in energy-dependent nutrient uptake across the jejunum that serves as the main site for absorption in the small intestine. This association has prompted us to investigate the bioenergetics underlying the alterations in jejunal absorption in 2,4,6-trinitrobenzenesulfonic acid-induced colitis in rats. We have found that mitochondrial oxygen consumption did not change in state 2 and state 3 respirations but showed an increase in state 4 respiration indicating a decrease in the respiratory control ratio of jejunal mitochondria during the peak of inflammation. This decrease in the coupling state was found to be guanosine diphosphate-sensitive, hence, implicating the involvement of uncoupling protein-2 (UCP2). Furthermore, the study has reported that the production of reactive oxygen species (ROS), known to be activators of UCP2, correlated negatively with UCP2 activity. Thus, we suggest that ROS production in the jejunum might be activating UCP2 which has an antioxidant activity, and that uncoupling of the mitochondria decreases the efficiency of energy production, leading to a decrease in energy-dependent nutrient absorption. Hence, this study is the first to account for an involvement of energy production and a role for UCP2 in the absorptive abnormalities of the small intestine in animal models of colitis.

中文翻译：

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TNBS诱发的结肠炎大鼠模型小肠中的线粒体生物能，解偶联蛋白2活性和活性氧产生。

炎症性肠病（IBD）通常与空肠中能量依赖性养分吸收的减少有关，空肠是小肠吸收的主要部位。这种联系促使我们研究大鼠2,4,6-三硝基苯磺酸诱导的结肠炎空肠吸收改变的生物能学。我们已经发现，状态2和状态3的呼吸中线粒体耗氧量没有变化，但是状态4的呼吸却增加了，这表明在炎症高峰期空肠线粒体的呼吸控制率降低了。发现偶联状态的这种降低是对鸟苷二磷酸敏感的，因此，牵涉到解偶联蛋白2（UCP2）的参与。此外，该研究报告说，活性氧物质（ROS）的产生（已知是UCP2的激活剂）与UCP2活性呈负相关。因此，我们认为空肠中的ROS产生可能是激活具有抗氧化活性的UCP2，而线粒体的解偶联会降低能量产生的效率，从而导致能量依赖性养分吸收的减少。因此，这项研究是第一个考虑到结肠炎动物模型中能量产生的参与和UCP2在小肠吸收异常中的作用的研究。线粒体的解偶联降低了能量产生的效率，导致能量依赖性养分吸收减少。因此，这项研究是第一个考虑到结肠炎动物模型中能量产生的参与和UCP2在小肠吸收异常中的作用的研究。线粒体的解偶联降低了能量产生的效率，导致能量依赖性养分吸收减少。因此，这项研究是第一个考虑到结肠炎动物模型中能量产生的参与和UCP2在小肠吸收异常中的作用的研究。