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目的:探讨Toll样受体4在小于胎龄儿生后发生胰岛素抵抗的作用。方法:建立动物模型,分为小于胎龄儿追赶生长组(S1组)、小于胎龄儿无追赶生长组(S2组)、适于胎龄儿组(AGA组)。生后4周和12周取血、肝脏和脂肪组织,检测血糖、胰岛素、甘油三酯、游离脂肪酸和总胆固醇,计算胰岛素抵抗指数(Homeostasis model assessment for insulin resistance index,HOMA-IR);ELISA法检测血清白介素-6、肿瘤坏死因子-α;实时定量RT-PCR法检测相同体质量肝脏和脂肪组织中Toll样受体4、髓细胞样分化因子88、核因子κB、肿瘤坏死因子-α和白介素-6 mRNA的表达。结果:与适于胎龄儿组和小于胎龄儿无追赶生长组相比,小于胎龄儿追赶生长组随年龄增长血糖、血清胰岛素、游离脂肪酸、甘油三酯和HOMA-IR逐渐增高(P<0.05),相同体质量肝脏和脂肪组织中Toll样受体4、髓细胞样分化因子88、核因子κB、肿瘤坏死因子-α和白介素-6 mRNA表达量也逐渐升高(P<0.05);肝脏和脂肪组织中Toll样受体4信号通路与胰岛素抵抗指数HOMA-IR呈显著正相关(P<0.05),脂肪组织中的相关性显著高于肝脏组织(P<0.05)。结论:SGA生后追赶生长者随年龄增长出现糖脂代谢异常;肝脏和脂肪组织Toll样受体4信号途径激活,诱发以TNF-α和IL-6为炎性介质的慢性炎症,促进胰岛素抵抗发生发展;脂肪组织在胰岛素抵抗发生发展中作用更强。
Objective: To investigate the effect of Toll-like receptor 4 on insulin resistance in children younger than gestational age. Methods: Animal models were established and divided into following-up group (S1 group), non-catch up group (S2 group) and gestational age group (AGA group). Blood, liver and adipose tissue were taken at 4 weeks and 12 weeks after birth, and blood glucose, insulin, triglyceride, free fatty acid and total cholesterol were measured. Homeostasis model assessment for insulin resistance index (HOMA-IR) Serum interleukin-6 and tumor necrosis factor-α were detected by real-time quantitative RT-PCR. Toll-like receptor 4, myeloid differentiation factor 88, nuclear factor κB, tumor necrosis factor-α Interleukin-6 mRNA expression. RESULTS: Compared with those who did not catch up in suitable gestational age group and those in small gestational age group, serum insulin, free fatty acid, triglyceride and HOMA-IR increased with increasing age (P <0.05). The expression of Toll-like receptor 4, myeloid differentiation factor 88, nuclear factor kappa B, tumor necrosis factor-alpha and interleukin-6 mRNA also increased gradually in the same body weight of liver and adipose tissue (P < There was a significant positive correlation between Toll-like receptor 4 signaling and insulin resistance index (HOMA-IR) in liver and adipose tissue (P <0.05) and adipose tissue (P <0.05). CONCLUSIONS: There is an abnormal glucose and lipid metabolism with increasing age following catch-up in SGA rats. Toll-like receptor 4 signaling in liver and adipose tissue is activated, inducing chronic inflammation with TNF-α and IL-6 as inflammatory mediators and promoting insulin resistance Development occurs; adipose tissue is more effective in the development of insulin resistance.