REGULATION OF INTESTINAL LIPID TRANSPORT

这个项目的主旨是了解 控制饮食脂质进入淋巴的输送。 的脂质 没有在淋巴中运输的进入储存池， 通过门静脉循环。 这些门脉脂质很可能是 由肝脏吸收，而不是由更多的外周组织吸收， 脂质在淋巴中运输。 肝脏部分分泌这些 膳食脂质作为VLDL。 VLDL催化剂的最终结果是LDL， 血浆中主要的胆固醇载体。 目前的建议首先寻求确定粘膜的大小， 中性脂质储存池对十二指肠内甘油三油酸酯输注的影响， 受生理操作如胆管插管的影响 这有望增加其大小和磷脂酰胆碱 共输注，这可能会减少它。池是孤立的，其 根据其酰基组成测定和表征其尺寸， BPLC和GLC方法。 由于存储池包含大量 内源性酰基，第二和第三个目的是确定 这些群体的起源。 通过静脉注射脂肪酸 （第二个目的）或乳糜微粒和VLDL残留物（第三个目的），粘膜 将测定这些脂质的摄取和 在不同的生理条件下调节摄取， 存储池预计会扩大或缩小。 第四个目标是 表征三酰基甘油的酰基组成， 乳糜微粒、VLDL、粘膜、储存池、微粒体和高尔基体 不同的生理条件。 将确定酰基 通过HPLC和GLC方法。 目的是比较酰基 每个隔间里的成分，试图了解 三酰甘油流在进入淋巴的 以乳糜微粒和极低密度脂蛋白为代表， 池 这可以通过三酰甘油组成的差异来揭示 在微粒体和高尔基体之间，高尔基体具有与 膳食脂质和具有酰基组成的微粒体 由更多的外源脂质组成。 第五个目的是检查膜 在不同淋巴水平下从微粒体到高尔基体的运动 三酰甘油转运 这些之间的囊泡交通效率 两种细胞器可能在肠道的能力中发挥作用， 运输脂质。 将使用脉冲追踪动力学。 的萌芽 来自微粒体的囊泡需要蛋白质酰化和 肠道这样做将在不同的条件下进行研究， 淋巴三酰甘油转运。酰基的来源 三酰甘油或磷脂酰胆碱将被研究， 酰基的选择，棕榈酸酯或油酸酯。

The major thrust of this project is to understand the factors that control the delivery of dietary lipids into the lymph. Lipids that are not transported in the lymph enter a storage pool and subsequently the circulation via the portal vein. These portal lipids are likely to be taken up by the liver rather than by more peripheral tissues as occurs with the lipids transported in lymph. The liver in part secretes these dietary lipids as VLDL. The end result of VLDL catabolism is LDL, the major cholesterol carrier in the plasma. The current proposal first seeks to determine the size of the mucosal neutral lipid storage pool on intraduodenal glyceryltrioleate infusion as influenced by physiological manipulations such as bile duct cannulation which is expected to increase its size and phosphatidylcholine co-infusion which is likely to decrease it. The pool is isolated, its size determined and characterized as to its acyl group composition using BPLC and GLC methodology. Since the storage pool contains considerable endogenous acyl groups, the second and third aim is to determine the origin of these groups. Using intravenous infusions of fatty acid (second aim) or chylomicron and VLDL remnants (third aim), the mucosa will be assayed for uptake of these lipids and the potential of regulating uptake under differing physiological conditions where the storage pool is expected to expand or contract. The fourth aim is to characterize the acyl group composition of the triacylglycerols in chylomicrons, VLDL, mucosa, storage pool, microsomes and Golgi under differing physiological conditions. The acyl groups will be determined by HPLC and GLC methodology. The object is to compare the acyl constituents in each compartment to try to understand where the triacylglycerol stream splits between that going into lymph as represented by chylomicrons and VLDL and that going into the storage pool. This may be revealed as differences in triacylglycerol composition between microsomes and Golgi with the Golgi having acyl groups similar to dietary lipids and the microsomes having an acyl group composition composed of more exogenous lipids. The fifth aim examines membrane movement from microsomes to Golgi under varying levels of lymphatic triacylglycerol transport. Vesicular traffic efficiency between these two organelles may play a role in the ability of the intestine to transport lipid. Pulse-chase kinetics will be used. The budding of vesicles from microsomes requires protein acylation and the ability of the intestine to do this will be studied under conditions of differing lymphatic triacylglycerol transport. The origin of the acyl group from triacylglycerol or phosphatidylcholine will be investigated as will the acyl group of choice, palmitate or oleate.