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Dietary fats and lipid aggregates in the intestinal lumen represent the processed forms of ingested triglycerides, phospholipids, and cholesterol that enter the gut after initial hydrolysis by lingual and gastric lipases. In the small intestine, bile salts emulsify these into smaller droplets, enabling pancreatic lipase and colipase to further break them down into fatty acids, monoglycerides, and micelles for diffusion across the enterocyte brush border.[1][2][3][5][9] Inside enterocytes, these components are re-esterified in the endoplasmic reticulum, packaged with apolipoprotein B into chylomicrons, and released basolaterally into lacteals for lymphatic transport to the bloodstream, bypassing initial liver processing.[2][3][9] This process supports systemic lipid distribution but, when dysregulated (e.g., via altered lymphatic permeability), contributes to diet-induced obesity and metabolic syndrome by promoting excessive fat uptake.[2] No drugs directly target these luminal aggregates; instead, therapeutic strategies focus on related pathways like bile acid recycling or lymphatic modulation in preclinical models.[2][5]
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