Tischler M E, Fagan J M
Metabolism. 1983 Sep;32(9):853-68. doi: 10.1016/0026-0495(83)90198-1.
Soft tissue injury to one hindlimb produced trauma in rats without affecting their food intake or weight gain. Histologic examination showed damage to the soleus and gastrocnemius muscles but not to the extensor digitorum longus muscle. The protein content of the injured soleus muscle was lower than that of the contralateral soleus at one day after injury, and was reflected in vitro by a faster rate of protein degradation. The injured soleus also showed greater rates of protein synthesis, glucose uptake, glycolysis, oxidation of glucose, pyruvate, and leucine, and de novo synthesis of alanine. During three days after the injury, urinary nitrogen excretion increased progressively and was paralleled by a faster rate of protein degradation in uninjured muscles incubated with glucose, insulin, and amino acids. In these muscles, the inhibition of protein degradation by insulin diminished, while its stimulation of protein synthesis was unaffected. This insensitivity of proteolysis to insulin in trauma can explain the increased rate of this process. The oxidation of glucose and pyruvate were lower in the diaphragms of traumatized than of normal rats incubated with leucine, while glycolysis and uptake of 2-deoxyglucose did not differ. The degradation of leucine and isoleucine was greater in the diaphragms of traumatized animals and was associated with a faster de novo synthesis of alanine. For the uninjured soleus muscles of the traumatized rats, the slower rates of oxidation of glucose, glycolysis, and uptake of 2-deoxyglucose in the presence of insulin showed an insensitivity of glucose metabolism to this hormone. In contrast, no differences were seen in these various metabolic processes between the extensor digitorum longus muscles of traumatized and normal rats. These data suggest that the response of skeletal muscles to trauma may depend on their physiologic and biochemical characteristics.
大鼠一侧后肢的软组织损伤造成了创伤，但未影响其食物摄入量或体重增加。组织学检查显示比目鱼肌和腓肠肌受损，但趾长伸肌未受损。损伤后一天，损伤的比目鱼肌蛋白质含量低于对侧比目鱼肌，体外表现为蛋白质降解速率加快。损伤的比目鱼肌还表现出更高的蛋白质合成、葡萄糖摄取、糖酵解、葡萄糖、丙酮酸和亮氨酸氧化以及丙氨酸从头合成速率。损伤后的三天内，尿氮排泄逐渐增加，同时，在与葡萄糖、胰岛素和氨基酸一起孵育的未损伤肌肉中，蛋白质降解速率加快。在这些肌肉中，胰岛素对蛋白质降解的抑制作用减弱，而其对蛋白质合成的刺激作用未受影响。创伤时蛋白水解对胰岛素的这种不敏感性可以解释这一过程速率的增加。与亮氨酸一起孵育时，创伤大鼠膈肌中葡萄糖和丙酮酸的氧化低于正常大鼠，而糖酵解和2-脱氧葡萄糖摄取没有差异。创伤动物膈肌中亮氨酸和异亮氨酸的降解更大，并且与丙氨酸更快的从头合成有关。对于创伤大鼠未损伤的比目鱼肌，在胰岛素存在下葡萄糖氧化、糖酵解和2-脱氧葡萄糖摄取的较慢速率表明葡萄糖代谢对这种激素不敏感。相比之下，创伤大鼠和正常大鼠的趾长伸肌在这些不同的代谢过程中没有差异。这些数据表明，骨骼肌对创伤的反应可能取决于其生理和生化特性。
