Leeuwenburgh C, Ji L L
University of Wisconsin-Madison, WI 53706, USA.
J Nutr. 1996 Jul;126(7):1833-43. doi: 10.1093/jn/126.7.1833.
The influences of food deprivation and refeeding on glutathione (GSH) status, antioxidant enzyme activity and lipid peroxidation in response to an acute bout of exercise were investigated in the liver and skeletal muscles of male Sprague-Dawley rats randomly divided into three groups: starved for 48 h without refeeding; starved for 48 h and refed for 24 or 48 h. Half of each group of rats was exercised on a treadmill until exhaustion and killed immediately, whereas the other half group was killed at rest. Food-deprived rats had significantly lower liver GSH concentration and GSH:glutathione disulfide (GSSG) ratio. Malondialdehyde concentrations in the liver and skeletal muscle were both higher in the starved than in the refed rats (P < 0.05). Refed rats had significantly greater liver GSH level, gamma-glutamylcysteine synthetase and glucose 6-phosphate dehydrogenase activities and plasma insulin concentration than unfed rats. Exercised 24- and 48-h refed rats had 27% and 31 % lower liver GSH (P < 0.05), respectively, and a 21 % lower GSH:GSSG ratio (P < 0.05) than their rested counterparts. Plasma insulin concentrations were significantly lower, whereas glucagon concentrations were greater in the exercised than in the rested rats. Muscle GSH concentration was significantly lower in the food-deprived than in the refed rats (P < 0.05) but was unaffected by exercise. Exercised 24-h refed rats had significantly elevated muscle GSSG concentration compared with rested rats, along with a higher GSH peroxidase and a lower gamma-glutamyltranspeptidase activity (P < 0.05). These data indicate that both food deprivation-refeeding and exhaustive exercise influence liver and skeletal muscle glutathione status and that these changes may be controlled by hepatic glutathione synthesis and release due to hormonal stimulation.
将雄性Sprague-Dawley大鼠随机分为三组，研究食物剥夺和再喂养对急性运动后肝脏和骨骼肌中谷胱甘肽（GSH）状态、抗氧化酶活性及脂质过氧化的影响：饥饿48小时且未再喂养；饥饿48小时后再喂养24或48小时。每组大鼠的一半在跑步机上运动至疲惫并立即处死，而另一半在休息时处死。食物剥夺的大鼠肝脏GSH浓度和GSH：谷胱甘肽二硫化物（GSSG）比值显著降低。饥饿大鼠肝脏和骨骼肌中的丙二醛浓度均高于再喂养大鼠（P<0.05）。再喂养大鼠的肝脏GSH水平、γ-谷氨酰半胱氨酸合成酶和葡萄糖6-磷酸脱氢酶活性以及血浆胰岛素浓度均显著高于未喂养大鼠。运动24小时和48小时的再喂养大鼠肝脏GSH分别比其休息的对应组低27%和31%（P<0.05），GSH：GSSG比值低21%（P<0.05）。运动大鼠的血浆胰岛素浓度显著较低，而胰高血糖素浓度则高于休息大鼠。食物剥夺大鼠的肌肉GSH浓度显著低于再喂养大鼠（P<0.05），但不受运动影响。与休息大鼠相比，运动24小时的再喂养大鼠肌肉GSSG浓度显著升高，同时谷胱甘肽过氧化物酶活性较高，γ-谷氨酰转肽酶活性较低（P<0.05）。这些数据表明，食物剥夺-再喂养和力竭运动均会影响肝脏和骨骼肌的谷胱甘肽状态，且这些变化可能受激素刺激引起的肝脏谷胱甘肽合成和释放的控制。
