Lang C H
Department of Surgery, State University of New York, Stony Brook, New York 11794-8191, USA.
Shock. 1996 Jan;5(1):22-7. doi: 10.1097/00024382-199601000-00006.
The purpose of the present study was to determine whether insulin-like growth factor (IGF)-I would increase whole body and muscle glucose uptake in septic rats that are known to be insulin resistant. Animals were infused with either saline, low-dose IGF-I, high-dose IGF-I, or a maximally stimulating dose of insulin for 2 h, and the glucose metabolic response was assessed using a euglycemic clamp in combination with [3-3H]glucose. Under basal conditions, sepsis increased the rates of whole body glucose uptake, glycolysis, and hepatic glucose production. Under euglycemic hyperinsulinemic conditions, septic rats demonstrated a marked insulin resistance as evidenced by the impaired rate of insulin-stimulated glucose uptake and muscle glycogen synthesis. In contrast, the infusion of either dose of IGF-I increased total glucose uptake, glycolysis, and glycogen synthesis in both control and septic rats to the same extent. Furthermore, there was no difference in the IGF-I stimulation of glucose uptake (as determined by [14C]-2-deoxyglucose) in the gastrocnemius, soleus, and heart between control and septic rats. These results indicate that the glucose metabolic response to IGF-I is intact in insulin-resistant septic rats.
本研究的目的是确定胰岛素样生长因子（IGF）-I是否会增加已知存在胰岛素抵抗的脓毒症大鼠的全身和肌肉葡萄糖摄取。给动物输注生理盐水、低剂量IGF-I、高剂量IGF-I或最大刺激剂量的胰岛素2小时，使用正常血糖钳夹结合[3-³H]葡萄糖评估葡萄糖代谢反应。在基础条件下，脓毒症增加了全身葡萄糖摄取、糖酵解和肝葡萄糖生成的速率。在正常血糖高胰岛素血症条件下，脓毒症大鼠表现出明显的胰岛素抵抗，胰岛素刺激的葡萄糖摄取和肌肉糖原合成速率受损证明了这一点。相比之下，输注任何一种剂量的IGF-I均使对照大鼠和脓毒症大鼠的总葡萄糖摄取、糖酵解和糖原合成增加到相同程度。此外，对照大鼠和脓毒症大鼠之间，IGF-I对腓肠肌、比目鱼肌和心脏葡萄糖摄取的刺激作用（由[¹⁴C]-2-脱氧葡萄糖测定）没有差异。这些结果表明，胰岛素抵抗的脓毒症大鼠对IGF-I的葡萄糖代谢反应是完整的。
