牛乳酸通过CD36/Fyn/FAK/mTORC1轴在牛乳腺上皮细胞中促进脂质合成
Xiaoru Yang1, Xinyue Lu2, Liping Wang1
1State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot 010021, China.
International journal of biological macromolecules
|October 14, 2023
概括
牛乳酸通过CD36和Fyn/FAK/mTORC1信号传递促进牛乳细胞中的脂质合成. 这一途径调节脂肪的产生,提供了对食脂肪酸利用的见解.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 动物科学动物科学
背景情况:
- 酸 (SA) 是一种和长链脂肪酸 (LCFA),对于奶牛的哺乳非常重要.
- 饮食中的SA储存为三糖醇 (TAG).
- 通过FAK/mTORC1信号传导,CD36 (脂肪酸转位酶) 在SA诱导的脂质合成中的作用尚不清楚.
研究的目的:
- 研究牛乳腺上皮细胞 (BMECs) 中CD36介导的酸诱导的脂质合成机制.
- 阐明FAK/mTORC1信号通路在这个过程中的参与.
主要方法:
- 在BMEC中使用了SA丰富补充剂.
- 使用了抗CD36抗体和CD36抑制剂SSO.
- 过度表达的CD36.
- 使用TAE226/拉帕米辛抑制了FAK/mTORC1.
- 进行了共免疫沉和酵母双杂交试验.
主要成果:
- 在BMEC中,SA增强了脂质合成和FAK/mTORC1通路活性.
- 抗CD36和SSO损害了SA诱导的脂质合成和信号;CD36过度表达增强了它.
- 抑制FAK/mTORC1降低了SA诱导的TAG合成和脂原基因表达.
- 确定了一个信号轴:CD36与Fyn相互作用,Fyn与FAK结合;FAK与TSC2相互作用,与mTORC1.1结合.
结论:
- 甜酸通过涉及Fyn/FAK/mTORC1信号的CD36依赖途径促进BMEC中的脂质生成.
- 这项研究揭示了乳腺细胞中LCFA诱导的脂质合成的新型分子机制.
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