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首页> 外文期刊>The Journal of Nutritional Biochemistry >10E12Z CLA alters adipocyte differentiation and adipocyte cytokine expression and induces macrophage proliferation.
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10E12Z CLA alters adipocyte differentiation and adipocyte cytokine expression and induces macrophage proliferation.

机译：10E12Z CLA改变脂肪细胞分化和脂肪细胞细胞因子表达，并诱导巨噬细胞增殖。

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摘要

The trans-10, cis-12 (10e12z) conjugated linoleic acid (CLA) isomer of CLA is responsible for loss of lipid storage or adipose tissue in vitro or in vivo. This isomer also induces inflammatory signaling in both mouse and human adipocytes in vitro. However, when these events occur and whether they are significant enough to affect other cell types are unclear. In these experiments, the 3T3-L1 cell line has been used to examine the interaction between inflammatory signaling and decreased differentiation or lipid storage induced by 10e12z CLA. In assays measuring both lipid accumulation and gene expression, differentiating 3T3-L1 cells exhibit concurrent induction of inflammatory signaling, as measured by cyclooxygenase-2 expression, and a decrease in adipocyte marker gene expression. Furthermore, in fully differentiated adipocytes, as identified in microarray assays and confirmed with real-time polymerase chain reaction, 10e12z CLA also significantly affected expression of both matrix metalloprotein-3 (MMP-3), collagen VI alpha 3 ColVI alpha 3 (VI alpha3) and the cytokine epiregulin, demonstrating that the effects of 10e12z broadly impact adipocyte function. In agreement with other experimental systems, 10e12z CLA inhibited RAW 264.7 cell proliferation; however, in response to adipocyte-conditioned media, 10e12z-CLA-treated adipocytes induced proliferation of this cell line, suggesting that the effect of 10e12z CLA is context dependent. These results are largely consistent with the known activation of the inflammatory mediator nuclear factor- kappaB in adipocytes in vitro and in vivo by 10e12z CLA treatment and demonstrate that adipose is an important target tissue of this isomer that impacts other cell types
机译：CLA的反式10，顺式12（10e12z）共轭亚油酸（CLA）异构体负责体内或体外脂质存储或脂肪组织的丢失。该异构体还在小鼠和人的脂肪细胞中诱导炎症信号。但是，尚不清楚何时发生这些事件以及它们是否显着足以影响其他细胞类型。在这些实验中，已将3T3-L1细胞系用于检查炎症信号与10e12z CLA诱导的分化降低或脂质存储减少之间的相互作用。在同时测量脂质蓄积和基因表达的试验中，分化的3T3-L1细胞表现出并发的炎症信号诱导（如环氧合酶2的表达所测量）和脂肪细胞标记基因表达的减少。此外，在微阵列分析中鉴定并通过实时聚合酶链反应证实的全分化脂肪细胞中，10e12z CLA还显着影响基质金属蛋白3（MMP-3），胶原蛋白VIα3 ColVI alpha 3（VI alpha3）的表达）和细胞因子上皮调节蛋白，证明10e12z的作用广泛影响脂肪细胞的功能。与其他实验系统一致，10e12z CLA抑制了RAW 264.7细胞的增殖。然而，响应于脂肪细胞条件培养基，经10e12z-CLA处理的脂肪细胞诱导了该细胞系的增殖，表明10e12z CLA的作用取决于环境。这些结果与通过10e12z CLA治疗在体内和体外脂肪细胞中炎症介质核因子-κB的已知活化基本一致，并表明脂肪是该异构体的重要靶标组织，会影响其他细胞类型

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