Laboratory of Molecular Biology of Exercise, School of Applied Sciences, University of Campinas, Limeira, Brazil.
Laboratory of Nutritional Genomics, School of Applied Sciences, University of Campinas, Limeira, Brazil.
J Endocrinol. 2019 Apr 1;241(1):59-70. doi: 10.1530/JOE-18-0567.
Non-alcoholic fatty liver disease (NAFLD) has a positive correlation with obesity, insulin resistance and type 2 diabetes mellitus (T2D). The aerobic training is an important tool in combating NAFLD. However, no studies have demonstrated the molecular effects of short-term strength training on the accumulation of hepatic fat in obese mice. This study aimed to investigate the effects of short-term strength training on the mechanisms of oxidation and lipid synthesis in the liver of obese mice. The short duration protocol was used to avoid changing the amount of adipose tissue. Swiss mice were separated into three groups: lean control (CTL), sedentary obese (OB) and strength training obese (STO). The obese groups were fed a high-fat diet (HFD) and the STO group performed the strength training protocol 1 session/day for 15 days. The short-term strength training reduced hepatic fat accumulation, increasing hepatic insulin sensitivity and controlling hepatic glucose production. The obese animals increased the mRNA of lipogenic genes Fasn and Scd1 and reduced the oxidative genes Cpt1a and Ppara. On the other hand, the STO group presented the opposite results. Finally, the obese animals presented higher levels of lipogenic proteins (ACC and FAS) and proinflammatory cytokines (TNF-α and IL-1β), but the short-term strength training was efficient in reducing this condition, regardless of body weight loss. In conclusion, there was a reduction of obesity-related hepatic lipogenesis and inflammation after short-term strength training, independent of weight loss, leading to improvements in hepatic insulin sensitivity and glycemic homeostasis in obese mice. Key points: (1) Short-term strength training (STST) reduced fat accumulation and inflammation in the liver; (2) Hepatic insulin sensitivity and HPG control were increased with STST; (3) The content and activity of ACC and content of FAS were reduced with STST; (4) STST improved hepatic fat accumulation and glycemic homeostasis; (5) STST effects were observed independently of body weight change.
非酒精性脂肪性肝病 (NAFLD) 与肥胖、胰岛素抵抗和 2 型糖尿病 (T2D) 呈正相关。有氧运动是对抗 NAFLD 的重要手段。然而，尚无研究表明短期力量训练对肥胖小鼠肝脂肪堆积的分子影响。本研究旨在探讨短期力量训练对肥胖小鼠肝脏氧化和脂质合成机制的影响。使用短时间方案避免改变脂肪组织的量。瑞士小鼠分为三组：瘦对照组 (CTL)、久坐肥胖组 (OB) 和力量训练肥胖组 (STO)。肥胖组给予高脂肪饮食 (HFD)，STO 组进行 1 次/天、持续 15 天的力量训练方案。短期力量训练可减少肝脂肪堆积，增加肝胰岛素敏感性并控制肝葡萄糖生成。肥胖动物增加了脂肪生成基因 Fasn 和 Scd1 的 mRNA，减少了氧化基因 Cpt1a 和 Ppara。另一方面，STO 组则呈现出相反的结果。最后，肥胖动物表现出更高水平的脂肪生成蛋白 (ACC 和 FAS) 和促炎细胞因子 (TNF-α 和 IL-1β)，但短期力量训练可有效降低这种情况，而与体重减轻无关。总之，短期力量训练可减少肥胖相关的肝脂肪生成和炎症，而与体重减轻无关，从而改善肥胖小鼠的肝胰岛素敏感性和血糖稳态。关键点：(1) 短期力量训练 (STST) 减少了肝脏脂肪堆积和炎症；(2) STST 增加了肝胰岛素敏感性和 HPG 控制；(3) 随着 STST，ACC 的含量和活性以及 FAS 的含量降低；(4) STST 改善了肝脂肪堆积和血糖稳态；(5) STST 的作用独立于体重变化。
