REGULATION OF INTESTINAL LIPID TRANSPORT

该项目的主旨是了解 控制饮食中的脂肪进入淋巴。脂类是 没有在淋巴中运输进入存储池，随后 通过门静脉循环。这些门脉脂质很可能是 被肝脏摄取，而不是被更多的外周组织摄取 脂类在淋巴中运输。肝脏部分地分泌这些 膳食中的脂类如极低密度脂蛋白。极低密度脂蛋白分解代谢的最终结果是低密度脂蛋白，即 血浆中的主要胆固醇携带者。 目前的建议首先试图确定粘膜的大小 中性脂肪储存池在十二指肠内输注甘油三油酸酯中的应用 受生理操作的影响，如胆管插管 预计会增加它的大小和卵磷脂 联合输液，这可能会减少它。泳池是隔离的，它的 根据其酰基组成测定并表征其尺寸 BPLC和GLC方法学。由于存储池包含相当大的 内源性酰基，第二和第三个目标是确定 这些群体的起源。使用静脉输注脂肪酸 (第二个目标)或乳杆菌和极低密度脂蛋白残留物(第三个目标)，粘膜 将被检测这些脂质的摄取和潜在的 在不同的生理条件下调节摄取 预计存储池将扩大或收缩。第四个目标是 三酰甘油的酰基组成的表征 乳糜粒、极低密度脂蛋白、粘膜、储存池、微粒子和高尔基体 不同的生理条件。将测定酰基 采用高效液相色谱(HPLC)和气相色谱(GLC)方法。目的是比较酰基 每个隔间的组成成分试图理解 三酰甘油在进入淋巴系统之间分流 以乳胶粒和极低密度脂蛋白为代表，进入仓库 游泳池。这可能是由于三酰甘油组成的差异所致。 在微粒体和高尔基体之间，高尔基体具有类似于 膳食脂质和具有酰基组成的微生物体 由更多的外源类脂组成。第五个目的是检膜 不同淋巴水平下微粒体向高尔基体的运动 三酰甘油的运输。这两个区域之间的泡状交通效率 两个细胞器可能在肠道的 转运脂。将使用脉冲追逐动力学。萌芽的…… 来自微粒体的囊泡需要蛋白质酰化和 这样做的肠道将在不同的条件下进行研究 淋巴三酰甘油的运输。酰基的来源是 三酰甘油或磷脂酰胆碱将被调查， 选择的酰基，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.