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Macronutrient absorption refers to the physiological process in the small intestine where carbohydrates, proteins, and fats from digested food are taken up by enterocytes primarily through transcellular transport mechanisms involving specific enzymes and transporters. Carbohydrates are broken down by brush-border enzymes like sucrase, maltase, and lactase into monosaccharides such as glucose, which are absorbed via sodium-glucose linked transporter 1 (SGLT1) or facilitated diffusion (e.g., GLUT5 for fructose); proteins are degraded by gastric pepsin, pancreatic proteases (trypsin, chymotrypsin), and peptidases into amino acids and di/tripeptides, absorbed mainly via PEPT1 proton-coupled transport; fats are emulsified by bile salts, hydrolyzed by pancreatic lipase into fatty acids and monoglycerides, and absorbed via micelles into enterocytes for chylomicron packaging. This process is essential for energy homeostasis but disruptions lead to malnutrition or metabolic disorders like obesity. While not a single molecular target, components such as SGLT1, PEPT1, and pancreatic lipase are modulated by drugs: liraglutide indirectly reduces absorption via delayed gastric emptying, orlistat blocks lipase, and acarbose inhibits carb-digesting enzymes, offering therapeutic avenues for obesity/diabetes management but posing risks like gastrointestinal side effects and vitamin malabsorption.
Inhibition of pancreatic lipase, Blockade of brush-border enzymes, Interference with sodium-coupled transporters
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