瘦素抵抗肥胖大鼠脂肪组织SOCS-3、PPARγ及ACO mRNA水平的探讨

目的观察高脂饮食诱导的肥胖瘦素抵抗大鼠细胞因子信号转导抑制因子-3(SOCS-3)、过氧化物酶体增殖物激活受体γ(PPARγ)及乙酰辅酶A氧化酶(ACO)mRNA表达水平的变化。方法30只Wistar雄性大鼠,6只为对照组喂饲基础饲料,24只为高脂组喂饲高脂饲料,第8周末按体重增量从高脂组中筛选出8只大鼠作为肥胖组,测定对照组和肥胖组大鼠血清瘦素,附睾脂肪组织中SOCS-3,PPARγ以及ACO mRNA表达。结果肥胖组大鼠体重以及血清瘦素水平均显著高于对照组(P<0.05);肥胖组脂肪组织SOCS-3、PPARγ mRNA水平显著高于对照组(P<0.05),而ACO mRNA则显著低于对照组(P<0.05)。结论高脂饮食诱导的肥胖大鼠存在瘦素信号转导通路的抑制,脂肪酸氧化能力降低,脂肪合成能力增强。

Study on SOCS-3, PPARγ and ACO mRNA expression of adipose tissues in obese rats with leptin resistance

OBJECTIVE: To study the difference of socs-3, PPARgamma and ACO mRNA expression in obese rats with leptin resistance induced by high-fat diet. METHODS: 6 Wistar male rats were fed with basic diet as control, and 24 rats were fed with high-fat diet as high-fat diet group. At the end of the 8th week, 8 obese rats were selected by body weight from high-fat diet group as obese group. Serum leptin, socs-3, PPARgamma and ACO mRNA were detected. RESULTS: In compare with control group, body weight, serum leptin, socs-3 and PPARgamma mRNA expressions of epididymal adipose tissues were significantly increased in obese group, while ACO mRNA were markedly decreased. CONCLUSION: Obese rats induced by high-fat diet showed the suppression of leptin signaling transduction pathway, decreases in fatty acid oxidation and increases in fat synthesis.