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Intestinal mixed micelles are supramolecular aggregates composed of bile salts, phospholipids, fatty acids, and cholesterol that form in the duodenal lumen during the digestion process [1, 2]. These complexes are essential for the solubilization of hydrophobic cholesterol molecules, enabling their transport across the unstirred water layer to the brush border of enterocytes, where protein transporters such as Niemann-Pick C1-Like 1 (NPC1L1) facilitate their uptake into the cell [3, 4]. By serving as the primary vehicle for both dietary and biliary sterol absorption, these mixed micelles play a pivotal role in maintaining systemic lipid homeostasis and contribute to the development of hypercholesterolemia when cholesterol levels are excessive [5, 10]. Pharmacological intervention often targets the physical and chemical properties of these micelles to reduce systemic cholesterol levels. Plant sterols and stanols lower serum cholesterol by competing with cholesterol for incorporation into the micelle core, thereby reducing the quantity of cholesterol available for intestinal absorption [6, 14]. Furthermore, bile acid sequestrants act by binding to the bile salts necessary for micelle formation, leading to the disruption of the micellar structure and increased fecal excretion of sterols [7, 9]. Understanding and manipulating micellar cholesterol solubility remains a key therapeutic strategy for managing cardiovascular disease and lipid disorders [12, 17].
Competitive displacement of cholesterol from the micellar phase and disruption of micelle formation via sequestration of essential bile acid components
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