炎症,氧化应激,线粒体功能与肥胖及其合并症的发展有关。这项研究的目的是评估通过限制卡路里来减轻体重对代谢谱的影响,炎症和氧化应激参数,肥胖人群的线粒体呼吸.总共109名受试者接受了两个周期的极低热量饮食与低热量饮食交替(24周)。我们分析了血清中的生化和炎症参数,以及氧化应激标志物,mRNA抗氧化基因表达,和外周血单核细胞(PBMC)的线粒体呼吸。干预之后,胰岛素抵抗和血脂都有改善,包括胆固醇亚组分。体重减轻导致线粒体ROSs含量显着降低,谷胱甘肽水平增加,再加上抗氧化系统的mRNA表达增强(SOD1,GSR,和CAT)。此外,显著改善基础耗氧量,最大呼吸,并观察到ATP的产生。这些发现表明,适度减肥可以改善胰岛素抵抗,脂质分布和细分,炎症和氧化应激参数,和线粒体呼吸。因此,我们可以肯定,饮食干预可以同时实现显著的体重减轻,并改善肥胖患者的代谢特征和线粒体功能。
Inflammation, oxidative stress, and mitochondrial function are implicated in the development of obesity and its comorbidities. The purpose of this study was to assess the impact of weight loss through calorie restriction on the metabolic profile, inflammatory and oxidative stress parameters, and mitochondrial respiration in an obese population. A total of 109 subjects underwent two cycles of a very low-calorie diet alternated with a low-calorie diet (24 weeks). We analyzed biochemical and inflammatory parameters in serum, as well as oxidative stress markers, mRNA antioxidant gene expression, and mitochondrial respiration in peripheral blood mononuclear cells (PBMCs). After the intervention, there was an improvement in both insulin resistance and lipid profiles, including cholesterol subfractions. Weight loss produced a significant reduction in mitochondrial ROSs content and an increase in glutathione levels, coupled with an enhancement in the mRNA expression of antioxidant systems (SOD1, GSR, and CAT). In addition, a significant improvement in basal oxygen consumption, maximal respiration, and ATP production was observed. These findings demonstrate that moderate weight loss can improve insulin resistance, lipid profiles and subfractions, inflammatory and oxidative stress parameters, and mitochondrial respiration. Therefore, we can affirm that dietary intervention can simultaneously achieve significant weight loss and improve metabolic profile and mitochondrial function in obesity.