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Effect of PPAR-delta agonist on the expression of visfatin, adiponectin, and resistin in rat adipose tissue and 3T3-L1 adipocytes

机译:PPAR-δ激动剂对大鼠脂肪组织和3T3-L1脂肪细胞中visfatin,脂联素和抵抗素表达的影响

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It has been recently reported that activation of PPAR-delta, by specific agonists or genetic manipulation, alleviates dyslipidemia, hyperglycemia, and insulin resistance in animal models of obesity and type 2 diabetes. The purpose of the present study was to determine whether the PPAR-delta agonist has a direct effect on adipokines in visceral adipose tissue of rats and in cultured adipocytes. We examined the expression of visfatin, adiponectin, and resistin mRNA in visceral adipose tissue of Wistar rats fed a high-fat diet and 3T3-L1 adipocytes treated with PPAR-delta agonist (L-165041). Body weight and biochemical measurements were performed. Rats fed a high-fat diet showed a greater increase in body weight than those fed a standard diet (P < 0.05), and treatment with L-165041 (10 mg/kg/day) significantly decreased weight gain (P < 0.05). The concentration of total cholesterol was lower, and HDL cholesterol was higher in L-165041-treated rats (P < 0.05). In the visceral adipose tissue of L-165041-treated rats, visfatin and adiponectin mRNA levels significantly increased compared to those of the untreated rats (P < 0.05). However, the expression of resistin decreased in the L-165041-treated rats. Furthermore, in cultured 3T3-L1 adipocytes, the level of visfatin and adiponectin mRNA was up-regulated in response to L-165041 treatment for nine days. By contrast, resistin mRNA levels were down-regulated by L-165041 treatment. The present study provides a novel evidence to suggest that the PPAR-delta agonist has regulatory effects on a variety of adipokines, and these effects might explain some of their metabolic function. (c) 2007 Elsevier Inc. All rights reserved.
机译:最近有报道,在肥胖症和2型糖尿病动物模型中,通过特异性激动剂或基因操作激活PPAR-δ可减轻血脂异常,高血糖和胰岛素抵抗。本研究的目的是确定PPAR-δ激动剂是否对大鼠内脏脂肪组织和培养的脂肪细胞中的脂肪因子有直接影响。我们检查了高脂饮食和经PPAR-δ激动剂(L-165041)处理的3T3-L1脂肪细胞的Wistar大鼠内脏脂肪组织中visfatin,脂联素和抵抗素mRNA的表达。进行体重和生化测量。饲喂高脂饮食的大鼠体重增加比饲喂标准饮食的大鼠更大(P <0.05),用L-165041(10 mg / kg /天)的治疗可显着降低体重增加(P <0.05)。在L-165041处理的大鼠中,总胆固醇浓度较低,而HDL胆固醇较高(P <0.05)。在L-165041处理的大鼠的内脏脂肪组织中,与未处理的大鼠相比,visfatin和脂联素mRNA水平显着增加(P <0.05)。但是,在L-165041处理的大鼠中,抵抗素的表达下降。此外,在培养的3T3-L1脂肪细胞中,响应9天的L-165041处理,visfatin和脂联素mRNA的水平上调。相反,通过L-165041处理,抵抗素mRNA水平被下调。本研究提供了新的证据,表明PPAR-δ激动剂对多种脂肪因子具有调节作用,这些作用可能解释了它们的某些代谢功能。 (c)2007 Elsevier Inc.保留所有权利。

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