Chapter 29: Digestion and Transport of Dietary Lipids

Dietary triacylglycerols undergo minimal enzymatic degradation in the mouth and stomach via lingual and gastric lipases, but the majority of lipid digestion occurs in the small intestine where pancreatic lipase, assisted by the cofactor colipase, hydrolyzes triglycerides into free fatty acids and 2-monoacylglycerols. Simultaneously, pancreatic phospholipase A2 cleaves phospholipids while cholesterol esterase hydrolyzes cholesterol esters, generating multiple lipid digestion products. Bile salts released from the gallbladder serve a critical emulsification function, increasing the surface area of lipid droplets and subsequently forming mixed micelles that solubilize these hydrophobic products alongside fat-soluble vitamins, facilitating their absorption across the enterocyte brush border. Within intestinal epithelial cells, absorbed fatty acids and monoacylglycerols are reesterified into triglycerides through the action of microsomal triglyceride transfer protein, which also facilitates assembly of mature chylomicrons containing apolipoprotein B-48. These nascent lipoproteins enter the lymphatic circulation before reaching systemic blood, where they acquire additional apolipoproteins including apoC-II and apoE through transfer from high-density lipoproteins. The mature chylomicron then circulates to peripheral tissues where apoC-II activates lipoprotein lipase on capillary endothelium, releasing fatty acids for oxidation in muscle or storage in adipose tissue, while the resulting chylomicron remnants enriched in cholesterol and apoE undergo hepatic uptake via receptor-mediated endocytosis. The chapter integrates clinical cases demonstrating pathological consequences of disrupted lipid processing, including gallstone-induced cholestasis with jaundice and fat malabsorption, alcohol-induced pancreatitis causing steatorrhea from pancreatic enzyme insufficiency, and inherited abetalipoproteinemia resulting from microsomal triglyceride transfer protein deficiency, preventing chylomicron assembly entirely. Additional therapeutic considerations include lipase-inhibiting drugs and non-digestible fat substitutes employed in weight management strategies.