Tso P, Balint J A
Am J Physiol. 1986 Jun;250(6 Pt 1):G715-26. doi: 10.1152/ajpgi.1986.250.6.G715.
Digestion of triglyceride in the intestine results in the production of 2-monoglyceride and fatty acid. Phosphatidylcholine is hydrolyzed in the lumen to form lysophosphatidylcholine before its absorption. These digestion products are absorbed by the enterocytes through simple diffusion. In contrast, cholesterol absorption seems specific and is energy dependent. After entry into the enterocytes, these lipid digestion products migrate to the endoplasmic reticulum. Both fatty acid-binding protein and sterol carrier protein may be involved in the intracellular transport of fatty acid and cholesterol, respectively. Through predominantly the monoglyceride pathway, monoglycerides and fatty acids are resynthesized to form triglyceride in the endoplasmic reticulum. The lipid droplets, coated with cholesterol, phospholipid, and apolipoproteins, are then further processed in the Golgi apparatus before being released by the enterocytes through exocytosis. As yet, little is known of the factors regulating the formation and release of these chylomicrons by the enterocytes. Although apolipoprotein B is a prerequisite for the formation of chylomicrons, the question of whether its supply is rate limiting for chylomicron formation remains to be demonstrated. Other factors that may play a role in chylomicron formation are luminal phospholipid supply, Ca2+, and microtubules. Chylomicrons and very low-density lipoproteins are probably produced by the enterocytes via different pathways. For example, Pluronic L-81, a hydrophobic surfactant, affects only chylomicron formation and has little effect on very low-density lipoprotein production. The movement of chylomicrons from the intercellular space through the basement membrane to the lamina propria is not fully understood. Once inside the lamina propria, the movement of chylomicrons is probably by diffusion and is greatly facilitated by interstitial hydration; thus the lymphogogic effect of fat absorption may serve an important function for the transfer of chylomicrons from the enterocytes to the lacteal.
肠道中甘油三酯的消化会产生2-单酰甘油和脂肪酸。磷脂酰胆碱在肠腔中被水解形成溶血磷脂酰胆碱后才被吸收。这些消化产物通过简单扩散被肠上皮细胞吸收。相比之下，胆固醇的吸收似乎具有特异性且依赖能量。进入肠上皮细胞后，这些脂质消化产物会迁移至内质网。脂肪酸结合蛋白和固醇载体蛋白可能分别参与脂肪酸和胆固醇的细胞内转运。通过主要的单酰甘油途径，单酰甘油和脂肪酸在内质网中重新合成形成甘油三酯。包裹着胆固醇、磷脂和载脂蛋白的脂滴，随后在高尔基体中进一步加工，然后由肠上皮细胞通过胞吐作用释放。目前，对于调节肠上皮细胞形成和释放这些乳糜微粒的因素知之甚少。虽然载脂蛋白B是乳糜微粒形成的先决条件，但其供应是否是乳糜微粒形成的限速因素仍有待证明。其他可能在乳糜微粒形成中起作用的因素包括肠腔磷脂供应、Ca2+和微管。乳糜微粒和极低密度脂蛋白可能由肠上皮细胞通过不同途径产生。例如，一种疏水性表面活性剂普朗尼克L-81仅影响乳糜微粒的形成，对极低密度脂蛋白的产生影响很小。乳糜微粒从细胞间隙穿过基底膜进入固有层的过程尚未完全了解。一旦进入固有层，乳糜微粒可能通过扩散移动，间质水化极大地促进了这种移动；因此，脂肪吸收的促淋巴作用可能对乳糜微粒从肠上皮细胞转移到乳糜管起着重要作用。
