Lipid–water interfaces and dietary lipid aggregates

Lipid–water interfaces and dietary lipid aggregates represent the physical and chemical environment where the digestion and absorption of dietary fats occur [1]. In the gastrointestinal tract, hydrophobic dietary lipids are emulsified by bile salts and phospholipids into smaller aggregates, such as micelles and droplets, creating a high surface area at the lipid–water interface [2]. This interface is the critical site for the adsorption and catalytic activity of lipolytic enzymes, most notably pancreatic lipase [3]. Interfacial activation is a phenomenon where these enzymes undergo conformational changes upon binding to the interface, exposing their active sites for substrate hydrolysis [3]. Drugs targeting this system typically aim to reduce fat absorption to treat obesity or manage lipid levels [4]. For example, lipase inhibitors like orlistat prevent the breakdown of triglycerides at these interfaces by binding to the enzyme's active site [4]. Bile acid sequestrants, such as colestyramine, interact with dietary lipid aggregates to disrupt the formation of micelles necessary for lipid solubilization and absorption [1]. Consequently, modulating these interfaces is a key strategy in metabolic disease management [4]. However, affecting these processes often leads to gastrointestinal side effects, such as steatorrhea, due to the presence of undigested fats in the colon [5]. Additionally, these drugs can interfere with the absorption of fat-soluble vitamins, necessitating nutritional monitoring [5].

Other names

Lipid-water interfaceDietary lipid aggregatesOil-water interfaceLipid micellesLipid emulsionsMixed micelles

Inhibition of interfacial lipolysis by preventing enzyme adsorption or catalytic activity at the lipid-water interface, and disruption of micellar solubilization of dietary fats.