IGF-I stimulates muscle glucose uptake during sepsis.
IGF-I stimulates muscle glucose uptake during sepsis.
复制标题
IGF-I 在败血症期间刺激肌肉葡萄糖摄取。
作者：
Charles H. Lang
本研究的目的是确定胰岛素样生长因子（IGF）-I是否会增加全身和肌肉葡萄糖摄取脓毒症大鼠是已知的胰岛素抵抗。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 h，并使用正葡萄糖钳夹结合[3- 3 H]葡萄糖评估葡萄糖代谢反应。在基础条件下，脓毒症增加全身葡萄糖摄取、糖酵解和肝脏葡萄糖产生的速率。在血糖正常的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糖原合成率受损证明。与此相反，输注任何剂量的IGF-I增加总葡萄糖摄取，糖酵解和糖原合成在控制和脓毒症大鼠相同的程度。此外，对照组和脓毒症大鼠的腓肠肌、比目鱼肌和心脏中IGF-I对葡萄糖摄取的刺激（通过[14 C]-2-脱氧葡萄糖测定）无差异。这些结果表明，胰岛素抵抗性脓毒症大鼠对IGF-I的葡萄糖代谢反应是完整的。
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.