Antunes Gabriel Calheiros, de Lima Robson Damasceno, Vieira Renan Fudoli Lins, Macêdo Ana Paula Azevêdo, Muñoz Vitor Rosetto, Zambalde Erika Pereira, Romeiro Caio Felipe, Simabuco Fernando Moreira, Prada Patricia Oliveira, da Silva Adelino Sanchez Ramos, Ropelle Eduardo Rochete, Cintra Dennys Esper, Pauli José Rodrigo
Laboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), São Paulo, Brazil.
Multidisciplinary Laboratory of Food and Health, State University of Campinas, Faculty of Applied Sciences, São Paulo, Brazil.
Clin Exp Pharmacol Physiol. 2022 Oct;49(10):1072-1081. doi: 10.1111/1440-1681.13687. Epub 2022 Jul 24.
Obesity is associated with low-grade inflammation and disturbances in hepatic metabolism. This study aimed to investigate the effects of resistance exercise on inflammatory signalling related to IκB kinase (IKK) ɛ protein (IKKɛ) and on hepatic fat accumulation in obese mice. Male Swiss mice were distributed into three groups: control (CTL) fed with standard chow; obese (OB) mice induced by a high-fat diet (HFD); obese exercised (OB + RE) mice fed with HFD and submitted to a resistance exercise training. The resistance exercise training protocol consisted of 20 sets/3 ladder climbs for 8 weeks, three times/week on alternate days. The training overload was equivalent to 70% of the maximum load supported by the rodent. Assays were performed to evaluate weight gain, hepatic fat content, fasting glucose, insulin sensitivity, IKKɛ phosphorylation and proteins related to insulin signalling and lipogenesis in the liver. Mice that received the high-fat diet showed greater adiposity, impaired insulin sensitivity, increased fasting glucose and increased hepatic fat accumulation. These results were accompanied by an increase in IKKɛ phosphorylation and lipogenesis-related proteins such as cluster of differentiation 36 (CD36) and fatty acid synthase (FAS) in the liver of obese mice. In contrast, exercised mice showed lower body weight and adiposity evolution throughout the experiment. In addition, resistance exercise suppressed the effects of the high-fat diet by reducing IKKɛ phosphorylation and hepatic fat content. In conclusion, resistance exercise training improves hepatic fat metabolism and glycaemic homeostasis, which are, at least in part, linked to the anti-inflammatory effect of reduced IKKɛ phosphorylation in the liver of obese mice.
肥胖与低度炎症及肝脏代谢紊乱有关。本研究旨在探讨抗阻运动对肥胖小鼠中与IκB激酶（IKK）ɛ蛋白（IKKɛ）相关的炎症信号传导以及肝脏脂肪堆积的影响。雄性瑞士小鼠被分为三组：喂食标准饲料的对照组（CTL）；由高脂饮食（HFD）诱导的肥胖（OB）小鼠；喂食HFD并接受抗阻运动训练的肥胖运动组（OB + RE）小鼠。抗阻运动训练方案包括8周内进行20组/3次阶梯攀爬，每周三次，隔日进行。训练负荷相当于啮齿动物所能承受最大负荷的70%。进行了相关测定以评估体重增加、肝脏脂肪含量、空腹血糖、胰岛素敏感性、IKKɛ磷酸化以及肝脏中与胰岛素信号传导和脂肪生成相关的蛋白质。接受高脂饮食的小鼠表现出更高的肥胖程度、受损的胰岛素敏感性、空腹血糖升高以及肝脏脂肪堆积增加。这些结果伴随着肥胖小鼠肝脏中IKKɛ磷酸化以及与脂肪生成相关的蛋白质如分化簇36（CD36）和脂肪酸合酶（FAS）的增加。相比之下，运动组小鼠在整个实验过程中体重和肥胖程度的增长较低。此外，抗阻运动通过降低IKKɛ磷酸化和肝脏脂肪含量抑制了高脂饮食的影响。总之，抗阻运动训练改善了肝脏脂肪代谢和血糖稳态，这至少部分与肥胖小鼠肝脏中IKKɛ磷酸化减少的抗炎作用有关。
