A topic in the Open Knowledge Graph — a free, open map of 15,290 topics and the order to learn them in.
Macronutrient digestion involves mechanical breakdown and enzymatic hydrolysis: carbohydrates are cleaved by salivary and pancreatic amylases then brush border enzymes into monosaccharides; proteins are denatured by stomach acid and hydrolyzed by pepsin, then pancreatic proteases into amino acids and small peptides; lipids are emulsified by bile salts and hydrolyzed by pancreatic lipase into fatty acids and monoglycerides. Absorption occurs primarily in the jejunum via enterocytes bearing microvilli (brush border) that increase absorptive area ~600-fold. Sugars and amino acids enter the portal circulation; long-chain fatty acids are packaged as chylomicrons and enter lymphatic lacteals before reaching the bloodstream.
Create a table with columns: nutrient class, enzymes, site of action, absorbed form, transport route. Then use clinical cases (celiac disease affecting villi, pancreatitis affecting enzyme secretion) to apply it.
By the time food reaches the small intestine, it has already been partially processed — chewed, mixed with salivary amylase in the mouth, and churned with stomach acid and pepsin in the stomach. But the small intestine, particularly the jejunum, is where the majority of nutrient digestion is completed and virtually all absorption occurs. Understanding this process requires tracking three separate nutrient classes — carbohydrates, proteins, and lipids — through their distinct enzymatic and transport pathways.
Carbohydrate digestion begins in the mouth with salivary amylase, which cleaves starch into smaller oligosaccharides. Pancreatic amylase continues this work in the duodenum. But amylases cannot break the final bonds between individual monosaccharides — that work falls to brush border enzymes (maltase, sucrase, lactase) embedded in the microvilli of enterocytes. These enzymes finish the job, releasing glucose, galactose, and fructose, which are then transported into enterocytes by SGLT1 (sodium-glucose co-transport) and GLUT5, cross the basolateral membrane via GLUT2, and enter the portal vein to reach the liver.
Protein digestion follows a similar pattern of enzyme relay. Stomach acid denatures proteins and converts pepsinogen to pepsin, which begins cleaving peptide bonds. In the duodenum, pancreatic proteases — trypsin, chymotrypsin, elastase, and carboxypeptidases — continue hydrolysis. Brush border peptidases complete the breakdown to amino acids and small di- and tripeptides. These are absorbed by specific transporters and also enter the portal circulation.
Lipid digestion requires an additional step: emulsification. Because fats are hydrophobic, they clump into large globules that offer minimal surface area for enzymes. Bile salts secreted from the liver (stored in the gallbladder) are amphipathic — they surround fat droplets and break them into tiny micelles, vastly increasing the surface available to pancreatic lipase. Lipase then cleaves triglycerides into fatty acids and monoglycerides. Inside enterocytes, long-chain fatty acids are reassembled into triglycerides, packaged into chylomicrons, and secreted into lymphatic lacteals — not the portal vein — traveling through the lymphatic system before entering the bloodstream near the heart.
The architectural feature that makes the jejunum so effective at absorption is the amplification of surface area at three scales: folds of Kerckring (large mucosal folds), villi (finger-like projections), and microvilli on enterocytes (the "brush border") combine to increase absorptive surface area roughly 600-fold compared to a smooth tube. Clinical disruptions to this architecture — villous atrophy in celiac disease, or lipase deficiency in pancreatitis — predictably impair absorption of specific nutrient classes in ways that directly map to the pathways described here.