Ferrara C M, Sherman W M, Leenders N, McCune S A, Roehrig K
School of Physical Activity and Human Services, Ohio State University, Columbus 43210, USA.
J Appl Physiol (1985). 1996 Oct;81(4):1670-6. doi: 10.1152/jappl.1996.81.4.1670.
The effects of a similar exercise training stimulus on maximal insulin-stimulated (MIS) plasma membrane glucose transporter number and glucose transport were determined in lean and obese SHHF/Mcc-facp rats. Six-week-old lean and obese male rats were randomly divided into four groups: lean sedentary (LSed), obese sedentary (OSed), lean exercise (LEx), and obese exercise (OEx). An 8- to 12-wk treadmill running program equalized daily muscular work for LEx and OEx. Plasma membranes were isolated from control and MIS muscles of mixed fiber types. MIS significantly increased glucose transport (3.4- and 2.8-fold) in LSed and OSed, respectively. MIS significantly increased glucose transporter number (2.5-fold) in LSed, but there was no increase in glucose transporter number in OSed. Peak oxygen uptake and citrate synthase activity were increased a similar amount for LEx and OEx groups, demonstrating a similar training stimulus. MIS significantly and similarly increased glucose transport in LEx and OEx (4.4- and 5.1-fold, respectively). The effects of MIS on plasma membrane glucose transporter number in the exercise-trained rats were similar to the responses observed in the sedentary lean and obese groups. MIS significantly increased glucose transporter number (2.6-fold) in LEx, whereas there was no increase in glucose transporter number in OEx. The reduction in MIS glucose transport in OSed appears to be related to a defect in the processes associated with the translocation of glucose transporters to the plasma membrane. Exercise training of the obese rats apparently did not alter this defect. Similar increases in peak oxygen uptake, citrate synthase, and MIS glucose transport in LEx and OEx groups suggest that insulin resistance does not limit the ability of the glucose transport system to adapt to exercise training in the obese male SHHF/Mcc-facp rats.
在瘦型和肥胖型SHHF/Mcc-facp大鼠中，确定了类似的运动训练刺激对最大胰岛素刺激（MIS）的质膜葡萄糖转运体数量和葡萄糖转运的影响。六周龄的瘦型和肥胖型雄性大鼠被随机分为四组：瘦型久坐组（LSed）、肥胖型久坐组（OSed）、瘦型运动组（LEx）和肥胖型运动组（OEx）。一个为期8至12周的跑步机跑步计划使LEx组和OEx组的每日肌肉工作量相等。从混合纤维类型的对照肌肉和MIS肌肉中分离质膜。MIS分别使LSed组和OSed组的葡萄糖转运显著增加（3.4倍和2.8倍）。MIS使LSed组的葡萄糖转运体数量显著增加（2.5倍），但OSed组的葡萄糖转运体数量没有增加。LEx组和OEx组的峰值摄氧量和柠檬酸合酶活性增加的幅度相似，表明训练刺激相似。MIS使LEx组和OEx组的葡萄糖转运显著且相似地增加（分别为4.4倍和5.1倍）。MIS对运动训练大鼠质膜葡萄糖转运体数量的影响与久坐的瘦型和肥胖组中观察到的反应相似。MIS使LEx组的葡萄糖转运体数量显著增加（2.6倍），而OEx组的葡萄糖转运体数量没有增加。OSed组中MIS葡萄糖转运的降低似乎与葡萄糖转运体向质膜易位相关过程中的缺陷有关。肥胖大鼠的运动训练显然没有改变这种缺陷。LEx组和OEx组中峰值摄氧量、柠檬酸合酶和MIS葡萄糖转运的类似增加表明，胰岛素抵抗并不限制肥胖雄性SHHF/Mcc-facp大鼠中葡萄糖转运系统适应运动训练的能力。
