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目的 探讨神经肽Y(NPY)Y5受体基因反义寡核苷酸脑室给药对饮食所致肥胖大鼠外周瘦素抵抗的影响。方法 (1)建立高营养饲料诱导的肥胖大鼠模型 ,侧脑室插管后注射NPYY5受体基因反义、错义寡核苷酸及生理盐水 ,观察大鼠腹膜后脂肪湿重的变化 ;(2 )采用ELISA双抗体夹心法测定血清瘦素含量、放免法测定血清胰岛素含量 ,RT PCR技术检测脂肪组织中ob基因的表达水平 ,评价该疗法对肥胖大鼠外周瘦素抵抗的影响。结果 经NPYY5受体基因反义寡核苷酸干预后 ,肥胖大鼠腹膜后脂肪湿重、血清胰岛素含量、血清瘦素含量、腹膜后脂肪组织ob基因mRNA表达水平均明显降低 ,除腹膜后脂肪组织湿重与肥胖错义组差异未达到统计学意义外 ,其余指标与肥胖盐水组、肥胖错义组相比差异均有显著性 ,而肥胖错义组与肥胖盐水组之间各观察指标差异均无显著性。结论 侧脑室注射NPYY5受体基因反义寡核苷酸可显著减少营养性肥胖大鼠的腹膜后脂肪 ,降低肥胖大鼠脂肪组织ob基因表达及血清瘦素、胰岛素含量 ,改善外周瘦素抵抗
Objective To investigate the effects of intraventricular administration of neuropeptide Y (NPY) Y5 receptor antisense oligonucleotide on peripheral leptin resistance in diet-induced obese rats. Methods (1) To establish a rat model of obesity induced by high-nutrition diet. After intracerebroventricular injection of NPYY5 receptor antisense, missense oligonucleotide and saline, the changes of peritoneal fat wet weight were observed. 2) Serum leptin levels were determined by ELISA double antibody sandwich method. Serum insulin levels were determined by radioimmunoassay. The ob gene expression in adipose tissue was detected by RT-PCR and the effect of the therapy on peripheral leptin resistance in obese rats was evaluated. Results After the intervention of NPYY5 receptor antisense oligodeoxynucleotide, the weight of retroperitoneal fat, serum insulin, serum leptin and mRNA expression of ob gene in retroperitoneal adipose tissue were significantly decreased in obese rats except for retroperitoneal fat The differences between the wet weight of the obese group and the obesity missense group did not reach the statistical significance, the other indexes were significantly different from those of the obesity saline group and the obesity missense group, while those of the obese missense group and the obese saline group were different No significant. Conclusion The intracerebroventricular injection of NPYY5 receptor gene antisense oligonucleotide can significantly reduce peritoneal fat in obese rats, reduce adip ob gene expression, serum leptin and insulin levels and improve peripheral leptin resistance in obese rats