Olefsky J M, Saekow M
Endocrinology. 1978 Dec;103(6):2252-63. doi: 10.1210/endo-103-6-2252.
The effects of changes in the amount of dietary carbohydrate (CHO) on cellular insulin and glucose metabolism have been assessed in rat adipocytes. Feeding animals a 67% CHO (fat-free) diet resulted in decreased insulin binding but enhanced activity of both the glucose transport system and intracellular pathways of glucose metabolism. Feeding rats a 67% fat (CHO-free) diet resulted in decreased insulin receptors as well as decreased activity of the glucose transport system and intracellular glucose metabolism. Therefore, the in vivo insulin resistance caused by a high fat, low CHO diet seems to be adequately explained, since all aspects of insulin's cellular action were depressed. On the other hand, at first approximation, the increased in vivo insulin response caused by a high CHO diet appears contradictory to the observed decrease in insulin binding. However, a probable explanation for this apparent paradox is provided by the enhanced activity of the cellular insulin effector systems distal to the insulin receptor. Therefore, the increased in vivo insulin responsiveness after high CHO feedings is most likely due to post receptor increases in various aspects of glucose metabolism.
在大鼠脂肪细胞中评估了膳食碳水化合物(CHO)含量变化对细胞胰岛素和葡萄糖代谢的影响。给动物喂食67%碳水化合物(无脂肪)饮食会导致胰岛素结合减少,但葡萄糖转运系统和葡萄糖代谢的细胞内途径活性增强。给大鼠喂食67%脂肪(无碳水化合物)饮食会导致胰岛素受体减少,以及葡萄糖转运系统和细胞内葡萄糖代谢活性降低。因此,高脂肪、低碳水化合物饮食引起的体内胰岛素抵抗似乎可以得到充分解释,因为胰岛素细胞作用的各个方面都受到了抑制。另一方面,初步看来,高碳水化合物饮食引起的体内胰岛素反应增加似乎与观察到的胰岛素结合减少相矛盾。然而,胰岛素受体远端的细胞胰岛素效应系统活性增强为这一明显的矛盾提供了一个可能的解释。因此,高碳水化合物喂养后体内胰岛素反应性增加最可能是由于受体后葡萄糖代谢各方面的增加。