CD36偶联mTORC1调控外源长链脂肪酸吸收和利用的机制

牛乳腺上皮细胞中乳脂合成所需18碳以上的长链脂肪酸全部由乳腺上皮细胞从血液中摄取，内转和利用其合成甘油三酯或其它乳脂成分。CD36是外源长链脂肪酸的膜转运器，但其作为受体促进乳脂合成的作用可能更为重要；mTORC1与乳脂合成密切相关，但CD36和mTORC1的关系目前并不清楚。我们在研究mTORC1在乳脂合成中的作用得到良好结果的基础上，力图通过本项目阐明CD36作为长链脂肪酸受体，通过FAK偶联mTORC1，构成CD36/FAK/mTORC1通路，提出新的与乳脂合成相关的长链脂肪酸信号转导模型。拟以硬脂酸（C18:0）作为外源刺激分子，通过分子细胞生物学技术和蛋白质组学技术阐明CD36/FAK/mTORC1通路、转录因子、外源长链脂肪酸吸收、去饱和、超长链脂肪酸和甘油三酯合成相关基因表达，以及产物形成之间的联系机制，为提高牛奶品质提供基础数据和技术支持。

All of 18 carbon atoms and longer long-chain fatty acids (LCFA) were required to uptake from blood for milk lipogenesis in bovine mammary epithelial cells, turn inward transport and esterification or desaturation to synthesize triglyceride and orther components of milk fat. CD36 is an exogenous LCFA membrane transporter, and it may play an important role in milk lipogenesis as a receptor of exogenous LCFA. It is realized that mTORC1 can regulate the synthesis of milk fat in various ways, but the relationship between CD36 and mTORC1 is not well known. This project aims to study the mechamism of CD36, FAK and mTORC1 forming the CD36/FAK/mTORC1 signaling pathway based on the results of the previous project which focus on the role of mTORC1 in milk lipogenesis. Here, we propose a new regulating model of LCFA signal transduction which related with synthesis of milk fat. Intended to be the role of molecular and cell biology as well as protomics techniques in relationship between CD36/FAK/mTORC1 pathway, transcription factors, and gene expresiion related with exogenous LCFA uptaking, turn inward transport, desaturation, synthesis of very long-chain fatty acids (VLCFAs) and triglyceride, and to discover the mechanism of products forming. The results obtained from this project will provide basic data and technical support to improve milk quality.