Wichterman K A, Chaudry I H, Baue A E
Arch Surg. 1979 Jun;114(6):740-5. doi: 10.1001/archsurg.1979.01370300094020.
Glucose intolerance occurs in patients with sepsis, and resistance to insulin has been thought to be part of this process. To study this phenomenon, peritonitis was produced in rats by cecal ligation and puncture. One group was killed ten hours later (early sepsis). A second group of rats was killed 16 to 24 hours after ligation, just prior to their expected death (late sepsis). Insulin stimulated glucose uptake to the same extent in muscles from rats in early sepsis, late sepsis, and from control rats. Even at an insulin concentration that produced submaximal stimulation of glucose uptake, no difference in glucose uptake between the three groups of muscles was observed. Thus, there was no resistance to the stimulatory action of insulin on glucose uptake by skeletal muscle during early and late sepsis. However, basal glucose uptake by isolated soleus muscle from animals in late sepsis was significantly increased compared with controls when these muscles were incubated in an aerobic environment. Under anaerobic conditions, glucose uptake in these two groups of muscles increased to the same level. This indicates that there is some stimulus that increases glucose uptake in late peritonitis and may explain the hypoglycemia of late experimental or untreated sepsis. This stimulus could be hypoxia or some other factor resulting from decreased blood flow and increased anaerobic metabolism.
脓毒症患者会出现葡萄糖耐量异常,胰岛素抵抗被认为是这一过程的一部分。为了研究这一现象,通过盲肠结扎和穿刺在大鼠中诱发腹膜炎。一组在10小时后处死(早期脓毒症)。第二组大鼠在结扎后16至24小时处死,恰好在它们预期死亡之前(晚期脓毒症)。胰岛素对早期脓毒症大鼠、晚期脓毒症大鼠和对照大鼠肌肉中葡萄糖摄取的刺激程度相同。即使在产生次最大葡萄糖摄取刺激的胰岛素浓度下,三组肌肉之间的葡萄糖摄取也没有差异。因此,在早期和晚期脓毒症期间,骨骼肌对胰岛素刺激葡萄糖摄取的作用不存在抵抗。然而,当在有氧环境中孵育时,晚期脓毒症动物分离的比目鱼肌的基础葡萄糖摄取与对照相比显著增加。在无氧条件下,这两组肌肉中的葡萄糖摄取增加到相同水平。这表明在晚期腹膜炎中有某种刺激增加了葡萄糖摄取,这可能解释了晚期实验性或未治疗脓毒症时的低血糖。这种刺激可能是缺氧或由于血流减少和无氧代谢增加导致的其他因素。