中文摘要：

目的探讨高脂喂养和脂质灌注诱导的胰岛素抵抗（IR）大鼠糖代谢、血浆抵抗素、脂联素水平和肌肉抵抗素蛋白表达的变化。方法分别采用高脂喂养和脂质灌注制造IR大鼠模型,用扩展胰岛素钳夹术评价胰岛素敏感性和糖代谢的变化,用酶联免疫法和斑点印迹法测定血浆脂联素及肌肉抵抗素水平。结果高脂喂养组（HF）大鼠基础血浆FFA水平明显高于对照组（NC）（P〈0.05）。钳夹稳态时,NC组和HF组FFA分别被抑制77%和56%,而脂质灌注组（L）FFA水平明显升高。HF和L组糖输注率明显低于NC组（P均〈0.01）,而L组又明显低于HF组（P〈0.05）;L组糖清除率也明显低于NC组（P〈0.01）。NC组肝糖输出率被抑制达85%,而HF和L组分别被抑制29%和9%。钳夹结束时,L组血浆抵抗素水平较基础值明显升高（P〈0.01）,且L组肌肉抵抗素水平明显高于NC组和HF组（P均〈0.05）。钳夹后各组脂联素水平均明显降低（P〈0.05）。结论脂质灌注和高脂喂养诱导了机体外周和肝组织的IR,但以前者更为明显,可能与抵抗素增加有关。

英文摘要：

Objective To investigate the changes of glucose metabolism, plasma resistin and adiponectin in insulin-resistant （IR） rats induced by high-fat diet and lipid infusion. Methods IR rats were induced by high-fat diet （HF group） and lipid infusion （L group）, respectively. Changes of insulin sensibility and glucose metabolism were evaluated by euglycaemic clamp technique combined with 3-^3 H glucose as a tracer. Plasma adiponectin and resistin levels, and resistin levels in muscle tissues were assessed by ELISA and dot-blot assay, respectively. Results In baseline, plasma free fatty acids （FFAs） levels were significantly increased in HF group compared with normal diet rats （N group, P〈0.05）. During clamp steadystate, the FFA levels were reduced by 77% and 56% in N and HF groups, respectively, with significant increase in L group. The glucose infusion rates （GIR） were obviously lower in HF and L groups than in N group （both P〈0.01）. Moreover,GIR was lower in L group than in HF group （P〈0.05）. The rate of glucose disappearance was significantly lower in L group than in N group. The hepatic glucose production in controls was suppressed by 85%, but only by 29% and 19% in HF and L group, respectively. After clamp, plasma resistin levels in L group were significantly increased compared with basal values （P〈0.01）. The resistin level of muscle tissues in L group was significantly higher than in N and HF groups （both P〈0. 05）. After clamp, the plasma adiponectin levels were all significantly decreased in all groups （P〈0. 05）. Conclusion Both lipid infusion and high-fat diet can induce peripheral and hepatic IR in rats, but IR in lipid-infused rats is more severe. This might be associated with elevated resistin.