Background Vaspin was recently identified as a novel adipokine that is predominantly secreted from adipose tissue and exerts insulin-sensitizing effects. This study was undertaken to elucidate the regulative effects of calorie control on the expression of vaspin and its potential mechanism.Methods Diet-induced obese Sprague Dawley （SD） rats were adopted as experimental models and accepted interventions of various ingestions and pioglitazone. Various differentiated stages of cultured 3T3-L1 cells were dealt with pioglitazone or TNFα in vitro for 48 hours to further verify findings in animal experiments.Results The rats were successfully induced into an obese experimental model with hyperinsulinemia, hyperlipidemia, and increased serum free fatty acid and TNFa by 12-week high-fat diet. It was found that depending on whether the rats were fed by a high-fat diet or a basal diet, there was extremely higher vaspin in the periepididymal fat pad than in subcutaneous adipose tissues by 16 weeks. Vaspin in sera and the periepididymal fat pad was much lower in rats with a high-fat diet than those with a basal diet （all P 〈0.05）, but vaspin in subcutaneous fat tissues was prone to increase in rats with a high-fat diet. A 4-week calorie restriction or pioglitazone on the obese rats resulted in a partial recovery of vaspin levels in sera and periepididymal adipose tissues, especially the latter revealed a more obvious superiority and increased vaspin levels of subcutaneous adipose. Surprisingly, the treatment of 4-week high-fat diet on non-obese rats did not significantly depress vaspin of sera and periepididymal adipose tissues. However, it is unknown if re-feeding generated the effect on vaspin levels of obese and non-obese rats on sera or adipose tissues. The correlation analysis showed that vaspin levels of serum and periepididymal fat tissues were negatively correlated with serum FFA, TNFα and insulin; meanwhile, there was a positive correlation between serum vaspin and vaspin of periepididymal fat tissues. Pi
WANG You-min WANG Wen-ping WANG Li-ping LU Qi-huan ZHOU Xiao-hui
目的:探讨腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)与LKB1在肥胖大鼠脂肪组织的表达及其对糖脂代谢的影响。方法:将30只6周龄雄性S-D大鼠随机分为普通饮食组(NC组)和高脂饮食组(HF组),各15只,分别予普通饲料喂养和高脂饲料喂养。喂养16周后,HF组大鼠体重高于NC组20%者为成功建立模型。所有大鼠过夜禁食后,麻醉状态下测量体重(BW),取静脉血测定血清游离脂肪酸(FFA)、甘油三酯(TG)、总胆固醇(TCH)、空腹血糖(FPG)、空腹胰岛素(FINS)。处死大鼠后,采用Western blot法测定各组大鼠骨骼肌组织中AMPKα、磷酸化AMPK(P-AMPKα)和磷酸化LKB1蛋白(P-LKB1)的表达。计算AMPK活性。结果:与NC组比较,HF组大鼠BW、FFA、TG、FPG、FINS均升高(P<0.05～P<0.01),脂联素水平降低(P<0.05),骨骼肌组织中P-AMPKα和P-LKB1蛋白表达降低,AMPK活性降低(P<0.05)。结论:高脂饮食诱导大鼠营养性肥胖,降低LKB1和AMPK的活性,从而导致TG和TCH的合成增加,血糖升高,形成胰岛素抵抗。
