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高脂饮食大鼠脂肪组织SOCS-3及FAS表达 被引量:9

Study on SOCS-3 and FAS expression of adipose tissues in rats fed with high-fat diet
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摘要 目的研究高脂饮食诱导产生的肥胖及肥胖抵抗大鼠脂肪组织细胞因子信号转导抑制因子-3(SOCS-3)及脂肪酸合成酶(FAS)的mRNA表达情况。方法Wistar雄性大鼠31只,其中7只喂饲普通基础饲料作为对照组;24只喂饲高脂饲料,第8周末,按体重增量从高脂饲料组筛选出5只大鼠作为肥胖组,5只大鼠作为肥胖抵抗组。测定血清甘油三酯和总胆固醇,检测附睾脂肪组织SOCS-3及FAS的mRNA表达。结果肥胖组大鼠血清甘油三酯及总胆固醇水平分别为(0.982±0.228),(2.213±0.364)mmol/L,均显著高于对照组大鼠的(0.717±0.153),(1.784±0.175)mmol/L(P<0.05),总胆固醇水平也显著高于肥胖抵抗组的(1.711±0.190)mmol/L(P<0.05);肥胖组大鼠的SOCS-3及FASmRNA表达水平均显著高于对照组和肥胖抵抗组(P<0.05)。结论高脂饮食诱导产生的肥胖和肥胖抵抗大鼠在基因表达调控上可能存在差异,肥胖大鼠的生脂能力增强并可能存在瘦素信号转导通路的抑制。 Objective To study the expression of suppressor of cytokine signaling 3 (SOCS -3 ) and fatty acid synthase( FAS ) mRNA of adipose tissue in obesity and obesity resistant rats induced by high-fat diet. Methods Seven male Wistar rats were fed with standard diet as control group and 24 rats fed with high-fat diet. After 8 weeks,5 rats as obesity group and 5 rats as obesity resistant group were selected by body weight increment from high-fat diet group. Serum triglyceride,total cholesterol,SOCS -3 and FAS mRNA of epididymal adipose tissues were detected. Results Serum triglyceride (0. 982 ±0. 228 mmol/L) and total cholesterol level (2. 213 ±0. 364 mmol/L) of obesity group were significantly higher than that of control (0. 717 ±0. 153,1. 784±0. 175 mmol/L,P 〈0. 05) ,and total cholesterol level was higher than that of obesity resistant group ( 1.711 ± 0. 190 mmol/L, P 〈 0.05 ). SOCS-3 and FAS mRNA of obesity group was also higher than that of control and obesity resistant group( P 〈 0.05 ). Conclusion Obesity rats and obesity resistant rats induced by highfat diet might be different in gene regulation, and obesity rats show both increased fat synthesis and possible suppression of leptin signaling transduction.
出处 《中国公共卫生》 CAS CSCD 北大核心 2009年第4期428-430,共3页 Chinese Journal of Public Health
基金 国家自然科学基金(30500409)
关键词 高脂饮食 肥胖 细胞因子信号转导抑制因子3(SOCS-3) 脂肪酸合成酶(FAS) high-fat diet obesity resistance suppressor of cytokine signaling 3 ( SOCS-3 ) fatty acid synthase ( FAS )
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