Rudwill Floriane, Bergouignan Audrey, Gastebois Caroline, Gauquelin-Koch Guillemette, Lefai Etienne, Blanc Stéphane, Simon Chantal
University of Strasbourg, IPHC, Strasbourg, France.
CNRS, UMR 7178, Strasbourg, France.
Liver Int. 2015 Jun;35(6):1700-6. doi: 10.1111/liv.12743. Epub 2015 Jan 21.
BACKGROUND & AIMS: Physical inactivity leads to a cluster of metabolic disorders that have been associated with non-alcoholic fatty liver diseases. We tested whether physical inactivity increases hepatic biomarkers of NAFLDs.
Sixteen normal-weight healthy women (body mass index = 21.2 ± 0.5 kg/m(2) ) were studied under controlled energy balance conditions during a previous 60-day bed rest with (n = 8) or without (n = 8) a combined aerobic/resistive exercise protocol. Stored samples were retrospectively used to measure plasma hepatic markers, i.e. steatosis-related alanine and aspartate transaminases, cytokeratin 18 and angiopoietin-like 3, at baseline, after 30 and 60 days of bed rest. Fasting insulin and triglycerides were measured at baseline and after 30 days of bed rest. Two indexes were calculated, one combining alanine and aspartate transaminase and cytokeratin 18 and another cytokeratin 18, homeostasis model assessment of insulin resistance and aspartate aminotransferase.
Sixty days of bed rest increased all hepatic markers (P < 0.05 for all) and the two indexes (P < 0.01 for both). Exercise significantly reduced the elevation in aspartate transaminase, cytokeratin 18 and both indexes (P < 0.02 for all) but not the increase in alanine transaminase and angiopoietin-like 3. Changes between baseline and 30 days of bed rest in triglycerides were positively associated with changes in aspartate transaminase (R(2) = 0.28, P = 0.04) suggesting a role of hypertriglyceridaemia in the alteration of liver metabolism under inactive conditions.
Physical inactivity increases, independent of fat mass, hepatic markers of steatosis and steatohepatitis. Regular exercise can limit these physical inactivity-induced metabolic alterations. Future studies need to elucidate the underlying mechanisms.
缺乏身体活动会导致一系列代谢紊乱,这些紊乱与非酒精性脂肪性肝病有关。我们测试了缺乏身体活动是否会增加非酒精性脂肪性肝病的肝脏生物标志物。
16名体重正常的健康女性(体重指数 = 21.2 ± 0.5 kg/m²)在之前为期60天的卧床休息期间,在能量平衡受控的条件下进行了研究,其中8名女性采用了有氧/抗阻联合运动方案,另外8名女性未采用该方案。回顾性地使用储存的样本,在卧床休息的第0天、30天和60天后测量血浆肝脏标志物,即与脂肪变性相关的丙氨酸和天冬氨酸转氨酶、细胞角蛋白18和血管生成素样3。在基线和卧床休息30天后测量空腹胰岛素和甘油三酯。计算了两个指标,一个是将丙氨酸和天冬氨酸转氨酶与细胞角蛋白18相结合,另一个是细胞角蛋白18、胰岛素抵抗稳态模型评估和天冬氨酸转氨酶。
60天的卧床休息使所有肝脏标志物升高(所有P < 0.05)以及两个指标升高(两者P < 0.01)。运动显著降低了天冬氨酸转氨酶、细胞角蛋白18及两个指标的升高幅度(所有P < 0.02),但未降低丙氨酸转氨酶和血管生成素样3的升高幅度。卧床休息第0天和30天之间甘油三酯的变化与天冬氨酸转氨酶的变化呈正相关(R² = 0.28,P = 0.04),这表明高甘油三酯血症在非活动状态下肝脏代谢改变中起作用。
缺乏身体活动会独立于脂肪量增加肝脏脂肪变性和脂肪性肝炎的标志物。规律运动可以限制这些由缺乏身体活动引起的代谢改变。未来的研究需要阐明其潜在机制。