Kostić Milan, Korićanac Goran, Tepavčević Snežana, Stanišić Jelena, Romić Snježana, Ćulafić Tijana, Ivković Tamara, Stojiljković Mojca
Department for Molecular Biology and Endocrinology, "Vinča" Institute of Nuclear Sciences-National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Metab Syndr Relat Disord. 2023 Mar;21(2):122-131. doi: 10.1089/met.2022.0078. Epub 2023 Jan 10.
Excessive fructose consumption along with a sedentary lifestyle provokes metabolic disorders and cardiovascular diseases. Fructose overload causes cardiac insulin resistance and increases reliance on fatty acid (FA) uptake and catabolism. The cardiometabolic benefits of exercise training have long been appreciated. The goal of the presented study is to shed a new light to the preventive role of exercise training on cardiac lipid metabolism in fructose-fed rats. Male Wistar rats were divided into control (C), sedentary fructose (F), and exercised fructose (EF) groups. Fructose was given as a 10% fructose solution in drinking water for 9 weeks. Low-intensity exercise training was applied for 9 weeks. The protein expression and subcellular localization of Lipin1, peroxisome proliferator-activated receptor α (PPARα), and peroxisome proliferator-activated receptor-γ coactivator 1 α (PGC1) were analyzed in the heart using blot. Cardiac forkhead box transcription factor 1 (FOXO1) and sirtuin 1 (SIRT1) protein levels were also evaluated. Gene expression of long-chain acyl-CoA dehydrogenase was analyzed by quantitative polymerase chain reaction. Exercise training has augmented the expression of main regulators of FA oxidation in the heart and achieves its effect by increasing the nuclear content of PPARα, Lipin1, and FOXO1 compared with the fructose group ( = 0.0422, = 0.000045, = 0.00958, respectively). In addition, Lipin1, FOXO1, and SIRT1 were increased in nuclear extract after exercise compared with the control group ( = 0.000043, = 0.0417, = 0.0329, respectively). In cardiac lysate, low-intensity exercise caused significantly increased protein level of PPARα, PGC1, FOXO1, and SIRT1 compared with control ( = 0.0377, = 0.0275, = 0.0096, = 0.0282, respectively) and PGC1 level compared with the fructose group ( = 0.0417). The obtained results imply that the heart with a metabolic burden additionally relies on FA as an energy substrate after low-intensity running.
过量摄入果糖以及久坐不动的生活方式会引发代谢紊乱和心血管疾病。果糖过载会导致心脏胰岛素抵抗，并增加对脂肪酸（FA）摄取和分解代谢的依赖。运动训练对心脏代谢的益处早已为人所知。本研究的目的是为运动训练对喂食果糖大鼠心脏脂质代谢的预防作用提供新的线索。雄性Wistar大鼠被分为对照组（C）、久坐果糖组（F）和运动果糖组（EF）。以10%的果糖溶液作为饮用水，喂食9周。进行9周的低强度运动训练。使用印迹法分析心脏中Lipin1、过氧化物酶体增殖物激活受体α（PPARα）和过氧化物酶体增殖物激活受体γ共激活因子1α（PGC1）的蛋白质表达和亚细胞定位。还评估了心脏叉头盒转录因子1（FOXO1）和沉默调节蛋白1（SIRT1）的蛋白质水平。通过定量聚合酶链反应分析长链酰基辅酶A脱氢酶的基因表达。与果糖组相比，运动训练增强了心脏中FA氧化主要调节因子的表达，并通过增加PPARα、Lipin1和FOXO1的核含量发挥作用（分别为=0.0422，=0.000045，=0.00958）。此外，与对照组相比，运动后核提取物中Lipin1、FOXO1和SIRT1增加（分别为=0.000043，=0.0417，=0.0329）。在心脏裂解物中，与对照组相比，低强度运动导致PPARα、PGC1、FOXO1和SIRT1的蛋白质水平显著升高（分别为=0.0377，=0.0275，=0.0096，=0.0282），与果糖组相比，PGC1水平升高（=0.0417）。获得的结果表明，在低强度跑步后，承受代谢负担的心脏额外依赖FA作为能量底物。
