Figure 1.

Triglyceride trafficking, storage, and mobilization in the small intestine. TGs are present in various pools in intracellular and extracellular spaces within the intestinal structure. Digestion products of dietary TGs are absorbed at the brush border across the apical membrane of the enterocyte. TG resynthesis through the MGAT (majority) or the G3P pathways occurs in the outer ER membrane. Lipid droplets formed in the ER membrane are packaged into pre-CMs that are transported in PCTVs to the Golgi for further processing. Mature CM particles exit the basolateral membrane via exocytosis of secretory vesicles. Lipid droplets in the ER membrane also may bud off to form CLDs that are recruited for CM synthesis during the interprandial period or are degraded in the autophagosome (APS). A putative, apical/subapical pool of lipid-poor apoB48 may be recruited for rapid CM secretion and replenished by lipid supply during the feeding–fasting cycle. Secreted CM particles move through the lamina propria, enter the lacteals, and are actively transported in lymphatic vessels of increasing size before being released into circulation. CM entry into lacteals occurs mainly through size exclusion, but certain prerequisites such as particular CM composition also play a role. SMC around the lacteal and larger lymphatic vessels, which may be modulated by neural inputs, VEGF-C, and other regulators, actively regulates lymph flow and CM transport to the circulation. CoA, coenzyme A; DG, diacylglycerol.