Egli Léonie, Lecoultre Virgile, Cros Jérémy, Rosset Robin, Marques Anne-Sophie, Schneiter Philippe, Hodson Leanne, Gabert Laure, Laville Martine, Tappy Luc
Department of Physiology, University of Lausanne, Lausanne, Switzerland;
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom; and.
Am J Clin Nutr. 2016 Feb;103(2):348-55. doi: 10.3945/ajcn.115.116988. Epub 2015 Dec 23.
Exercise prevents the adverse effects of a high-fructose diet through mechanisms that remain unknown.
We assessed the hypothesis that exercise prevents fructose-induced increases in very-low-density lipoprotein (VLDL) triglycerides by decreasing the fructose conversion into glucose and VLDL-triglyceride and fructose carbon storage into hepatic glycogen and lipids.
Eight healthy men were studied on 3 occasions after 4 d consuming a weight-maintenance, high-fructose diet. On the fifth day, the men ingested an oral (13)C-labeled fructose load (0.75 g/kg), and their total fructose oxidation ((13)CO2 production), fructose storage (fructose ingestion minus (13)C-fructose oxidation), fructose conversion into blood (13)C glucose (gluconeogenesis from fructose), blood VLDL-(13)C palmitate (a marker of hepatic de novo lipogenesis), and lactate concentrations were monitored over 7 postprandial h. On one occasion, participants remained lying down throughout the experiment [fructose treatment alone with no exercise condition (NoEx)], and on the other 2 occasions, they performed a 60-min exercise either 75 min before fructose ingestion [exercise, then fructose condition (ExFru)] or 90 min after fructose ingestion [fructose, then exercise condition (FruEx)].
Fructose oxidation was significantly (P < 0.001) higher in the FruEx (80% ± 3% of ingested fructose) than in the ExFru (46% ± 1%) and NoEx (49% ± 1%). Consequently, fructose storage was lower in the FruEx than in the other 2 conditions (P < 0.001). Fructose conversion into blood (13)C glucose, VLDL-(13)C palmitate, and postprandial plasma lactate concentrations was not significantly different between conditions.
Compared with sedentary conditions, exercise performed immediately after fructose ingestion increases fructose oxidation and decreases fructose storage. In contrast, exercise performed before fructose ingestion does not significantly alter fructose oxidation and storage. In both conditions, exercise did not abolish fructose conversion into glucose or its incorporation into VLDL triglycerides. This trial was registered at clinicaltrials.gov as NCT01866215.
运动可通过尚不清楚的机制预防高果糖饮食的不良影响。
我们评估了以下假设,即运动通过减少果糖转化为葡萄糖和极低密度脂蛋白(VLDL)甘油三酯以及果糖碳储存到肝糖原和脂质中,来预防果糖诱导的VLDL甘油三酯增加。
八名健康男性在食用维持体重的高果糖饮食4天后,分3次进行研究。在第5天,这些男性口服(13)C标记的果糖负荷(0.75 g/kg),并在餐后7小时内监测他们的总果糖氧化((13)CO2产生)、果糖储存(果糖摄入量减去(13)C-果糖氧化)、果糖转化为血液中(13)C葡萄糖(果糖糖异生)、血液VLDL-(13)C棕榈酸酯(肝脏从头脂肪生成的标志物)和乳酸浓度。在一种情况下,参与者在整个实验过程中一直躺着[仅果糖处理,无运动条件(NoEx)],在另外两种情况下,他们在果糖摄入前75分钟进行60分钟的运动[运动,然后果糖条件(ExFru)]或在果糖摄入后90分钟进行运动[果糖,然后运动条件(FruEx)]。
FruEx组的果糖氧化显著高于ExFru组(46%±1%)和NoEx组(49%±1%)(P<0.001)。因此,FruEx组的果糖储存低于其他两种情况(P<0.001)。各条件下果糖转化为血液中(13)C葡萄糖、VLDL-(13)C棕榈酸酯和餐后血浆乳酸浓度无显著差异。
与久坐状态相比,果糖摄入后立即进行运动可增加果糖氧化并减少果糖储存。相反,果糖摄入前进行运动不会显著改变果糖氧化和储存。在这两种情况下,运动均未消除果糖转化为葡萄糖或其掺入VLDL甘油三酯。该试验已在clinicaltrials.gov上注册,注册号为NCT01866215。