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Food entering the human gut is, at the molecular level, a tangle of biopolymers — starch, proteins, triglycerides, nucleic acids — that the body's own enzymes did not synthesise and the cells lining the gut cannot absorb intact. Digestion is the controlled, multi-stage hydrolysis of these polymers into their constituent monomers; absorption is the subsequent transport of those monomers across the intestinal epithelium into the blood and lymph. The entire process is performed by a tubular organ ~9 m long, lined with an exchange surface that — through villi and microvilli — is amplified to roughly 200 m² in an adult. This lesson surveys the anatomy of the gut, the mechanical and chemical phases of digestion, the regulated zymogen activation of pancreatic enzymes, the absorption of carbohydrates, proteins and fats, and the disorders that disrupt each stage. The intestine is the textbook application of every Lesson 0 principle: vast surface area, short diffusion distance, steep gradient maintained by blood and lymph flow.
This lesson maps to AQA 7402 Section 3.3.3 — Digestion and absorption (refer to the official AQA specification document for exact wording). The specification requires that students understand digestion of carbohydrates, proteins and lipids in mammals; the role of bile salts in lipid digestion; the absorption of monomers across the ileum epithelium, including co-transport of glucose and amino acids with sodium ions, and the formation of chylomicrons in the absorption of lipid.
The mammalian digestive tract is a hollow tube ~9 m long, opened at both ends, running from mouth to anus. Specialised regions perform sequential functions.
flowchart TD
M[Mouth<br/>mechanical mastication<br/>salivary amylase<br/>mucus lubrication]
M --> O[Oesophagus<br/>peristalsis only<br/>no digestion]
O --> S[Stomach<br/>HCl + pepsin<br/>protein denaturation<br/>partial digestion]
S --> D[Duodenum<br/>pancreatic enzymes<br/>bile<br/>main chemical digestion]
D --> J[Jejunum<br/>nutrient absorption]
J --> I[Ileum<br/>further absorption<br/>vitamin B12, bile salts]
I --> LI[Large intestine<br/>water + electrolyte absorption<br/>microbial fermentation]
LI --> R[Rectum + anus<br/>storage and elimination]
Mastication (chewing) by molars mechanically breaks food into smaller particles, increasing surface area for enzymatic attack. Salivary glands secrete saliva containing salivary amylase (which begins hydrolysis of starch to maltose at pH ~7) and mucin (a glycoprotein that lubricates the food bolus for swallowing). Saliva contains essentially no protease or lipase activity, so protein and fat digestion does not begin in the mouth.
The oesophagus is a muscular tube ~25 cm long, lined with stratified squamous epithelium for mechanical protection. Peristalsis — sequential contraction of circular and longitudinal smooth muscle layers — propels the bolus to the stomach. No digestive enzymes are secreted; salivary amylase continues acting on starch within the bolus until the acidic stomach environment denatures it.
The stomach is a muscular bag with three smooth muscle layers (longitudinal, circular, oblique) producing churning rather than purely linear peristalsis. The lining contains four secretory cell types: parietal cells secrete hydrochloric acid (pH ~1.5); chief cells secrete the inactive zymogen pepsinogen; mucous cells secrete a protective mucus + bicarbonate layer; G cells secrete the hormone gastrin which stimulates further acid secretion.
Low stomach pH performs three functions: (i) it denatures dietary proteins, exposing internal peptide bonds for enzymatic attack; (ii) it activates pepsinogen by cleaving an inhibitory N-terminal segment, generating active pepsin (an endopeptidase cleaving internal peptide bonds preferentially at aromatic residues); (iii) it kills most ingested microorganisms, providing innate immune protection. Pepsin functions optimally at pH 1.5–2.0 — a unique adaptation because most enzymes denature at such low pH; pepsin has evolved disulfide-bridge-stabilised tertiary structure that survives the acidic environment in which it must operate.
The small intestine is the principal site of chemical digestion and absorption. It comprises three regions:
The large intestine (caecum, colon, rectum, ~1.5 m) absorbs water and electrolytes from the residual chyme, compacting it into faeces. The colon harbours a dense microbial community (~10¹³ organisms) that ferments dietary fibre to short-chain fatty acids, synthesises vitamin K and B vitamins, and contributes to colonic epithelial nutrition.
Mechanical digestion comprises chewing, churning by the stomach, and mixing by intestinal smooth muscle. It increases the surface area of food particles, accelerating enzymatic hydrolysis but does not break chemical bonds. Chemical digestion is the enzyme-catalysed hydrolysis of biopolymers to monomers, breaking specific covalent bonds and consuming water.
The two are complementary: mechanical action without chemical action would leave food undigested at the molecular level; chemical action on a large bolus would be slow because surface-to-volume ratio of the food limits enzyme access. A common A-Level error is to treat digestion as a single stage; in fact it is multi-organ, multi-stage and integrates mechanical, chemical and hormonal processes.
Dietary carbohydrate is principally starch (~50 % of energy intake in typical Western diets), with smaller contributions from sucrose, lactose and dietary fibre.
The end products of carbohydrate digestion are therefore glucose, fructose and galactose — three monosaccharides ready for absorption.
Dietary protein is hydrolysed by a sequence of endopeptidases (which cleave internal peptide bonds, breaking long chains into shorter peptides) and exopeptidases (which cleave terminal residues, releasing free amino acids).
The zymogen activation cascade is a classic example of biological proenzyme safety. Inactive zymogens are synthesised in the pancreatic acinar cells, packaged in zymogen granules, and exported to the duodenum without ever encountering the substrate; activation occurs only in the duodenal lumen by enterokinase. If activation occurs prematurely within the pancreas (as in acute pancreatitis triggered by gallstones or alcohol), the gland digests itself, producing severe abdominal pain and a 5–10 % mortality.
Triglycerides — the major dietary lipid — present a special problem: they are insoluble in water, so digestion in the aqueous lumen requires an emulsification step before enzymatic attack.
The lacteal pathway is unique to lipid absorption; carbohydrates and amino acids enter blood capillaries directly. This is a frequent A-Level distractor: candidates writing that "all absorbed nutrients enter the hepatic portal vein" are incorrect — chylomicrons bypass the liver on their first pass.
flowchart TD
V[Villus<br/>~1 mm projection]
V --> EC[Enterocytes<br/>columnar epithelium<br/>microvilli on apical surface]
V --> CAP[Capillary network<br/>fenestrated endothelium<br/>drains to hepatic portal vein]
V --> LAC[Lacteal<br/>blind-ended lymphatic<br/>chylomicron drainage]
V --> SM[Smooth muscle fibre<br/>villus contraction<br/>mixes apical fluid]
EC --> MV[Microvilli ~1 μm<br/>brush border<br/>200 m² total SA]
The villus is a finger-like projection of mucosa ~1 mm tall. Each villus contains a capillary network (draining via the hepatic portal vein to the liver), a central lacteal (draining to the thoracic duct), smooth muscle fibres that contract intermittently to mix the apical fluid, and a covering of columnar enterocytes. Each enterocyte bears ~3,000 microvilli — apical membrane projections ~1 μm long, ~0.1 μm wide — collectively called the brush border. The microvilli amplify the surface area of the small intestine roughly 600-fold; the resulting total absorptive surface is ~200 m². Embedded in the microvillar membrane are the brush-border enzymes (maltase, sucrase, lactase, peptidases) and the transport proteins for glucose, amino acids, peptides and fatty acids.
Glucose and galactose are absorbed across the apical membrane of the enterocyte by SGLT1 (sodium-glucose linked transporter 1), a symporter that couples the inward movement of one glucose (or galactose) to the inward movement of two Na⁺ down its electrochemical gradient. The Na⁺ gradient is maintained by the basolateral Na⁺/K⁺-ATPase, which pumps 3 Na⁺ out and 2 K⁺ in per ATP hydrolysed. Glucose accumulated inside the enterocyte then exits the basolateral membrane via GLUT2 (a facilitated diffusion transporter) into the interstitial fluid, and from there into the capillary blood.
This is secondary active transport: the active step is Na⁺/K⁺-ATPase consuming ATP; the glucose uptake is driven by the Na⁺ gradient that the pump establishes. The mechanism allows glucose to be absorbed against its concentration gradient — essential when luminal glucose is depleted late in a meal.
Fructose is absorbed across the apical membrane by GLUT5, a facilitated diffusion transporter that does not require Na⁺. Fructose cannot be absorbed against its concentration gradient, which limits the capacity for fructose uptake and explains why high-fructose diets cause osmotic diarrhoea.
Amino acids are absorbed by multiple Na⁺-coupled symporters (one family for neutral, another for basic, another for acidic amino acids). Small dipeptides and tripeptides are absorbed by PEPT1, an H⁺-coupled symporter, and then hydrolysed to amino acids inside the enterocyte. Free amino acids exit the basolateral membrane via Na⁺-independent facilitated transporters and enter the hepatic portal blood.
Monoglycerides and fatty acids diffuse passively across the lipid bilayer or are taken up by specific transporters. They are resynthesised to triglycerides inside the enterocyte and packaged into chylomicrons for lacteal export.
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