失血性休克后的慢性组织胰岛素抵抗。
Chronic tissue insulin resistance following hemorrhagic shock.
作者信息
Ryan N T, George B C, Egdahl D H, Egdahl R H
出版信息
Ann Surg. 1974 Oct;180(4):402-7. doi: 10.1097/00000658-197410000-00004.
Abstract
Metabolism of fat and muscle tissue was measured for 30 days following shock and reinfusion in rabbits. Tissue insulin resistance in the post-shock period was demonstrated by decreased oxidation of glucose and decreased incorporation of glucose into neutral lipid or glycogen during incubation with insulin. In addition, the insulin stimulated incorporation of amino acids into muscle protein was markedly reduced after shock. Conversely, the capacity of muscle to oxidize leucine was enhanced by shock, even in the presence of insulin. Tissue insulin resistance and increased leucine catabolism are likely to contribute to the general metabolic response to shock and trauma.
摘要
在兔子遭受休克和再灌注后的30天内，对脂肪和肌肉组织的代谢进行了测量。休克后时期的组织胰岛素抵抗表现为，在与胰岛素一起孵育期间，葡萄糖氧化减少，葡萄糖掺入中性脂质或糖原的量减少。此外，休克后胰岛素刺激的氨基酸掺入肌肉蛋白的过程明显减少。相反，即使存在胰岛素，休克也会增强肌肉氧化亮氨酸的能力。组织胰岛素抵抗和亮氨酸分解代谢增加可能有助于对休克和创伤的总体代谢反应。
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