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A dietary fat micelle is a transient, spherical aggregate formed in the small intestine during digestion of dietary fats. After emulsification of dietary triglycerides and other hydrophobic lipids by bile salts, digestive enzymes break fats into fatty acids, monoglycerides, cholesterol, and fat-soluble vitamins. These products are surrounded by bile salts and phospholipids, forming micelles. Micelles have a hydrophilic surface and a hydrophobic core, which allows otherwise insoluble lipids to be solubilized in the aqueous environment of the intestines and transported to the brush border of enterocytes. At the enterocyte surface, micelle components diffuse out and are absorbed. Micelle formation is essential for normal dietary absorption of long-chain fatty acids, cholesterol, and fat-soluble vitamins. Micelles are not a protein, gene, or classical drug target but a physical carrier necessary for lipid absorption. Disruption of micelle formation (e.g. absence of bile, pancreatic insufficiency, or after certain drug interventions) leads to fat malabsorption. The term “dietary fat micelle” is not used in biomedical literature to designate a molecular target. Instead, it describes a structural/physiological process central to the absorption of dietary lipids, not a molecule or biological structure that can be modulated by specific drugs or therapeutic agents in a conventional sense.
Orlistat: inhibits pancreatic lipase, preventing triglyceride breakdown and thus impairing micelle formation and fat absorption. Bile acid sequestrants: bind bile acids, reducing availability of bile for micelle formation, impeding fat absorption.
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