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Activation of liver X receptor (LXR) enhances de novo fatty acid synthesis in bovine mammary epithelial cells

机译:肝X受体(LXR)的激活增强了牛乳腺上皮细胞的从头脂肪酸合成

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摘要

Liver X receptor (LXR) is a nuclear receptor and a known regulator of lipid synthesis in rodents; however, the role of LXR in the regulation of fatty acid synthesis in bovine mammary epithelial cells has not yet been defined. The objective of the study was to evaluate the effect of LXR activation on the de novo synthesis of fatty acids in bovine mammary epithelial cells (BME-UV). Bovine mammary epithelial cells were treated with T0901317 (T09), an LXR agonist. Treatment of BME-UV with T09 increased the transcription of ATP-binding cassette transporter-G1, an LXR target gene, without modifying LXRα mRNA abundance. Acute and chronic treatment of BME-UV with T09 dramatically increased de novo fatty acid synthesis. Activation of LXR resulted in the upregulation of transcription, translation, and proteolytic cleavage of sterol regulatory element-binding protein-1 (SREBP1), a lipogenic transcription factor expressed in the bovine mammary gland. Additionally, the mRNA abundance of fatty acid synthase, an LXR and SREBP1 target gene, increased in response to LXR activation. Our data indicate that SREBP1 is regulated by LXR activation in BME-UV. Controlling LXR activation may prove useful in regulating milk fat production in lactating dairy cows.
机译:肝脏X受体(LXR)是一种核受体,是啮齿动物类脂合成的已知调节剂。然而,LXR在调节牛乳腺上皮细胞脂肪酸合成中的作用尚未确定。这项研究的目的是评估LXR活化对牛乳腺上皮细胞(BME-UV)中脂肪酸从头合成的影响。牛乳腺上皮细胞用LXR激动剂T0901317(T09)处理。用T09处理BME-UV可以增加ATP结合盒转运蛋白G1(一种LXR靶基因)的转录,而不会改变LXRαmRNA的丰度。用T09急性和慢性治疗BME-UV可以显着增加从头脂肪酸的合成。 LXR的激活导致固醇调节元件结合蛋白1(SREBP1)(一种在牛乳腺中表达的脂肪生成转录因子)的转录,翻译和蛋白水解切割上调。此外,响应LXR激活,脂肪酸合酶,LXR和SREBP1目标基因的mRNA丰度增加。我们的数据表明,SREBP1受BME-UV中LXR激活的调节。控制LXR活化可能在调节泌乳奶牛的乳脂生产中很有用。

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