Weight-loss-independent benefits of exercise on liver steatosis and stiffness in Japanese men with NAFLD.

Weight-loss-independent benefits of exercise on liver steatosis and stiffness in Japanese men with NAFLD.
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DOI:
10.1016/j.jhepr.2021.100253
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发表时间:
2021-06
期刊:
JHEP reports : innovation in hepatology
影响因子:
--
通讯作者:
Shoda J
Shoda J
中科院分区:
其他
文献类型:
--
作者:
Oh S;Tsujimoto T;Kim B;Uchida F;Suzuki H;Iizumi S;Isobe T;Sakae T;Tanaka K;Shoda J

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据报道,运动对非酒精性脂肪肝病(NAFLD)的治疗具有与减肥无关的有益效果,但其潜在机制尚不清楚。为了帮助确定这一机制,回顾性研究了运动对个体组织(肝脏、脂肪组织和骨骼肌)的影响。对患有 NAFLD 的日本肥胖男性进行为期 3 个月的锻炼方案的数据进行了分析,并将其与旨在实现减肥的 3 个月的饮食限制计划中的数据进行了比较。在较小的子队列中研究了潜在的机制。与体重减轻的影响无关,运动方案每减轻 1% 的体重,可使肝脏脂肪变性减少 9.5%,肝脏僵硬度减少 6.8%,并导致 FibroScan-AST 评分降低 16.4%。这些肝脏参数的改善与人体测量变化(脂肪组织减少和肌肉质量保存)、肌肉力量增加(+11.6%)、炎症和氧化应激减少(铁蛋白:-22.3%和硫代巴比妥酸:-12.3%)以及有机因子浓度变化(硒蛋白-P:-11.2%, 运动期间,卵泡抑素:+17.1%,脂联素:+8.9%,肌肉生长抑制素:-21.6%。此外,氧化应激传感器转录因子Nrf2的靶基因在单核细胞中表达较高,表明Nrf2被激活。大量高强度运动可有效进一步减少肝脏脂肪变性并增强病理生理参数(肝酶活性和有机因子谱)的改善。运动与减肥无关的益处包括对 NAFLD 患者肝脏的抗脂肪变性和抗僵硬作用。这些益处似乎是通过改变器官间串扰获得的,其特点是改善有机因子失衡以及减少炎症和氧化应激。我们研究了运动对与减肥无关的非酒精性脂肪肝(NAFLD)的影响。我们发现,运动通过多种机制对肝脏具有相当大的与减肥无关的益处。这表明运动对于 NAFLD 患者很重要,无论他们是否减肥。运动对肝脏脂肪变性和僵硬有影响,与体重减轻无关。运动可以维持肌肉质量并改变有机因子的分泌。运动会增加库普弗细胞的吞噬能力并激活 Nrf2。应积极进行运动,尤其是剧烈运动来控制非酒精性脂肪肝(NAFLD)。
A weight-loss-independent beneficial effect of exercise on non-alcoholic fatty liver disease (NAFLD) management has been reported, but the underlying mechanism is unknown. To help determine this mechanism, the effects of exercise on individual tissues (liver, adipose tissue, and skeletal muscle) were retrospectively studied. Data from Japanese obese men with NAFLD in a 3-month exercise regimen were analysed and compared with those in a 3-month dietary restriction program designed to achieve weight loss. The underlying mechanism was studied in a smaller subcohort. Independent of the effect of weight loss, the exercise regimen reduced liver steatosis by 9.5% and liver stiffness by 6.8% per 1% weight loss, and resulted in a 16.4% reduction in FibroScan-AST score. Improvements in these hepatic parameters were closely associated with anthropometric changes (reduction in adipose tissue and preservation of muscle mass), increases in muscle strength (+11.6%), reductions in inflammation and oxidative stress (ferritin: -22.3% and thiobarbituric acid: -12.3%), and changes in organokine concentrations (selenoprotein-P: -11.2%, follistatin: +17.1%, adiponectin: +8.9%, and myostatin: -21.6%) during the exercise regimen. Moreover, the expression of target genes of the transcription factor Nrf2, an oxidative stress sensor, was higher in monocytes, suggesting that Nrf2 is activated. Large amounts of high-intensity exercise were effective at further reducing liver steatosis and potentiating improvements in pathophysiological parameters (liver enzyme activities and organokine profiles). The weight-loss-independent benefits of exercise include anti-steatotic and anti-stiffness effects in the livers of patients with NAFLD. These benefits seem to be acquired through the modification of inter-organ crosstalk, which is characterised by improvements in organokine imbalance and reductions in inflammation and oxidative stress. We investigated the effects of exercise on non-alcoholic fatty liver disease (NAFLD) that were not related to weight loss. We found that exercise had considerable weight-loss-independent benefits for the liver through a number of mechanisms. This suggests that exercise is important for NAFLD patients, regardless of whether they lose weight. Exercise has effects on liver steatosis and stiffness, independent of weight loss. Exercise maintains muscle mass and alters the secretion of organokines. Exercise increases the phagocytic capacity of Kupffer cells and activates Nrf2. Exercise, especially vigorous exercise, should be used aggressively to manage non-alcoholic fatty liver disease (NAFLD).
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