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目的观察高脂饮食肥胖大鼠血清瘦素,胰岛素水平及下丘脑细胞因子信号转导抑制因子-3基因(suppressors-of-cytokine-signaling 3,SOCS-3)表达变化及其关系,探讨高脂饮食肥胖大鼠引发瘦素抵抗及胰岛素抵抗的发生机制。方法以高脂饮食制备幼年雄性肥胖大鼠模型,采用放射免疫法检测各组大鼠血清瘦素、胰岛素及C肽浓度,葡萄糖氧化酶法检测血清葡萄糖水平,利用RT-PCR技术检测各组大鼠下丘脑SOCS-3基因表达水平。结果 (1)高脂饮食诱导的肥胖组大鼠体重明显高于对照组;(2)肥胖组大鼠血清瘦素、胰岛素,血糖及C肽水平明显升高,与对照组比较均有显著性差异;(3)肥胖组大鼠下丘脑SOCS-3的mRNA水平明显高于对照组;(4)肥胖组大鼠下丘脑内SOCS-3 mRNA水平分别与血清瘦素、胰岛素含量呈显著正相关。结论高脂饮食诱导的肥胖大鼠可出现瘦素抵抗和胰岛素抵抗以及SOCS-3基因表达上调。SOCS-3基因表达上调使瘦素及胰岛素受体后JAK-STAT信号转导通路抑制,可能参与了瘦素及胰岛素抵抗的发生机制。
Objective To observe the changes of serum leptin and insulin levels and the expression of hypothalamic suppressors-of-cytokine-signaling 3 (SOCS-3) in obese rats fed with high-fat diet and to explore the relationship between hyperlipidemia Mechanism of Leptin Resistance and Insulin Resistance Induced by Diet in Obese Rats. Methods The juvenile male obesity rat model was induced by high-fat diet. The levels of serum leptin, insulin and C-peptide were measured by radioimmunoassay. The serum glucose level was detected by glucose oxidase method. Rat hypothalamus SOCS-3 gene expression levels. Results (1) The body weight of obese rats induced by high-fat diet was significantly higher than that of the control group. (2) Serum leptin, insulin, blood glucose and C-peptide levels were significantly increased in the obesity group compared with the control group (3) The mRNA level of SOCS-3 in the hypothalamus of obese rats was significantly higher than that of the control rats; (4) The levels of SOCS-3 mRNA in hypothalamus of obese rats were positively correlated with serum leptin and insulin . Conclusion Leptin resistance and insulin resistance and up-regulation of SOCS-3 gene expression may occur in obese rats induced by high-fat diet. Up-regulation of SOCS-3 gene inhibits the JAK-STAT signal transduction pathway of leptin and insulin receptor, which may be involved in the mechanism of leptin and insulin resistance.