Digestion breaks food down. Absorption gets it into the body. Follow a glucose molecule from the inside of your small intestine all the way to a liver cell — and find out exactly why our patient from Lesson 11 is malnourished despite eating well.
Content from this lesson that appears directly in HSC Biology exams
Explaining how the structure of the small intestine maximises absorption surface area is tested in nearly every HSC paper — 3–5 marks in Section II. Must link finger-like projections → increased SA → more transport proteins → faster absorption rate.
Distinguishing glucose/amino acid absorption (capillary → portal vein → liver) from fatty acid absorption (lacteals → lymph → bloodstream) is a commonly tested 2–3 mark question. Must name the lacteal and explain why fats take a different route.
The liver's role in regulating blood glucose (glycogen storage), amino acid processing (deamination, urea), and lipid metabolism. Appears as 2–3 mark application questions, often linked to homeostasis in Module 3.
Role of the colon in water reabsorption and faeces formation tested as 1–2 mark short answer. Common exam application: explaining why diarrhoea causes dehydration, or why constipation produces hard faeces.
The Absorption Surface
Three levels of folding create an extraordinary surface area
The small intestine faces a fundamental SA:V challenge identical to the one we explored in gas exchange (L10) — it needs to absorb nutrients from a relatively small tube into the bloodstream as efficiently as possible. Evolution's solution is the same: fold a large surface area into a small space. But in the small intestine, this folding happens at three distinct scales simultaneously.
The inner wall of the small intestine is not smooth — it is thrown into large circular folds called plicae circulares (valves of Kerckring). These folds triple the surface area compared to a smooth tube and slow the passage of chyme, giving more time for absorption.
The surface of each plica is covered in thousands of villi — finger-like projections of the intestinal epithelium. Each villus contains a central capillary network and a lacteal (lymph vessel). The villus structure increases surface area by a further 10×. This is the scale where most absorption occurs.
Each epithelial cell on a villus has its own surface covered in microvilli — tiny hair-like projections visible only under electron microscopy. These form the "brush border" and increase surface area by a further 20×. The combined effect of all three levels of folding gives the small intestine a total surface area of approximately 250m² — roughly the size of a tennis court.
Each villus epithelial cell (enterocyte) is also packed with the transport proteins needed to move glucose, amino acids, and ions across the membrane — and has abundant mitochondria to power the active transport required.
Follow the Molecule
Every stop from the intestinal lumen to your bloodstream
Digestion has done its job — the lumen of your small intestine now contains glucose, amino acids, fatty acids, glycerol, vitamins, minerals, and water. Here is what happens next, step by step, for a single glucose molecule.
Glucose floats free in the watery contents of the small intestine lumen, produced by the action of maltase on maltose. Concentration of glucose here is high — just produced by digestion. Concentration in the enterocyte cell is lower. This gradient initially favours passive diffusion, but the bulk of glucose absorption requires active transport.
Glucose crosses the brush border membrane of the enterocyte via sodium-glucose co-transport (SGLT1) — a carrier protein that moves one glucose molecule and two Na⁺ ions together from lumen into cell. This is secondary active transport: the Na⁺ gradient (maintained by Na⁺/K⁺ ATPase pumps on the other side of the cell) provides the energy to pull glucose in, even when glucose concentration inside is already high.
Glucose is now inside the absorptive epithelial cell. It moves through the cytoplasm toward the basolateral (blood-side) membrane. The enterocyte's many mitochondria power the ion pumps that maintain the Na⁺ gradient required for continued co-transport. Glucose does not linger here — the cell is a throughway, not a store.
Glucose exits the enterocyte through the basolateral membrane via GLUT2 — a facilitated diffusion transporter (no ATP needed here because glucose moves down its concentration gradient from cell into the blood). It immediately enters the capillary network that runs through the villus core.
Capillaries from all the villi drain into the hepatic portal vein — a blood vessel that carries nutrient-rich blood directly from the intestine to the liver before it enters general circulation. This is a critical checkpoint: the liver gets first access to all absorbed nutrients.
Glucose processed by the liver enters the hepatic vein, then the inferior vena cava, then the heart, and from there is pumped through systemic arteries to every cell in the body. Every cell that needs glucose — muscle, brain, kidney — takes it up from the blood. This is how a bite of bread eventually fuels a contracting muscle fibre.
Why fatty acids bypass the portal vein and travel via lymph
Fatty acids and glycerol — the products of fat digestion — cannot simply enter capillaries the way glucose and amino acids do. They are hydrophobic: they repel water and would disrupt blood plasma if released directly into capillaries in large quantities. Instead, fats take a completely different absorption route.
Unlike glucose, fatty acids are lipid-soluble — they simply dissolve through the phospholipid bilayer of the enterocyte brush border membrane by passive diffusion. No transporter needed. This is one of the few cases in nutrient absorption where simple diffusion is the primary mechanism.
Once inside the enterocyte, fatty acids and glycerol are reassembled into triglycerides in the smooth endoplasmic reticulum. These triglycerides are then packaged with cholesterol and proteins into large particles called chylomicrons by the Golgi apparatus.
Chylomicrons are too large to enter capillaries directly. Instead they are secreted into the lacteal — the blind-ended lymph vessel running through the core of each villus. Lacteals have large gaps between their endothelial cells that allow chylomicrons to enter. Lymph from the lacteals drains into the lymphatic system.
Lymph carrying chylomicrons travels through the lymphatic system and empties into the thoracic duct, which drains into the left subclavian vein — bypassing the liver entirely for first pass. Fat-soluble vitamins (A, D, E, K) also travel this route, packaged with chylomicrons.
What happens to what you can't absorb
By the time intestinal contents pass from the small intestine into the large intestine, essentially all useful nutrients have been absorbed. What remains is a watery mixture of indigestible material (dietary fibre, dead cells, bacteria), water, electrolytes, and bile pigments. The large intestine's job is to recover as much water and electrolyte as possible before elimination.
The colon absorbs approximately 1.3–1.8 litres of water per day from intestinal contents. Water follows sodium ions that are actively pumped out of the colon lumen into the bloodstream — osmosis then pulls water out passively. Electrolytes (Na⁺, K⁺, Cl⁻) are also recovered. This is why the colon's contents gradually thicken from liquid to semi-solid faeces as they move through.
The large intestine contains over 1000 species of resident bacteria (gut microbiome) that ferment undigested material — primarily dietary fibre. Fermentation produces short-chain fatty acids (absorbed and used as energy), gases (methane, CO₂ — responsible for flatulence), and vitamins K and B12 that are absorbed here.
The remaining material — indigestible fibre, dead bacteria (~30% of faecal mass), dead intestinal cells, bile pigments (giving faeces its brown colour), mucus, and small amounts of fat and protein — is compacted into faeces in the rectum. Defecation is triggered by rectal distension, controlled by the internal (involuntary) and external (voluntary) anal sphincters.
You now have everything you need
Return to the patient from Lesson 11. You now have the biological knowledge to explain every one of her symptoms precisely. Here is the resolution.
Activities
In your book, draw a single villus in cross-section and longitudinal section. Label: microvilli (brush border), enterocytes, capillary network, lacteal, basement membrane, and smooth muscle. Annotate each with one function. Then answer the questions below.
Type here or answer in your book.
| Nutrient | Mechanism crossing brush border | Enters (capillary or lacteal?) | Route to systemic blood | Passes through liver first? |
|---|---|---|---|---|
| Glucose | ||||
| Amino acids | ||||
| Fatty acids | ||||
| Water |
Type here or answer in your book.
Assessment
Select the best answer — feedback shown immediately
1. Why do fatty acids enter the lacteal rather than the capillary after absorption?
2. Glucose crosses the brush border of enterocytes via sodium-glucose co-transport (SGLT1). Which of the following correctly explains the energy source for this process?
3. Which of the following correctly traces the route of absorbed amino acids from the intestinal lumen to systemic circulation?
4. Diarrhoea can cause dangerous dehydration even when a patient continues to drink water. Which explanation best accounts for this?
5. A drug blocks the enzyme that assembles triglycerides in enterocytes. Which of the following correctly predicts the result?
6. Explain how the structure of the small intestine is adapted to maximise nutrient absorption. In your answer, refer to three structural features at different scales and explain how each increases absorption efficiency. 5 MARKS
Three scales: plicae → villi → microvilli. Each needs structure + function + why it improves efficiency.
7. Compare the absorption routes of glucose and fatty acids. In your answer, identify where each enters the transport system, the vessel type involved, and whether each passes through the liver before entering systemic circulation. 4 MARKS
Two routes × two marks each — structure + hepatic portal comparison
8. Explain the role of the large intestine in maintaining water balance in the body. In your answer, describe the mechanism of water reabsorption and explain what happens when this process is disrupted. 3 MARKS
1. B — Fatty acids are reassembled into triglycerides and packaged into chylomicrons inside the enterocyte. Chylomicrons are too large (~80–1200nm) to squeeze through the tight junctions of blood capillary endothelium. Lacteals have looser endothelial junctions that accommodate chylomicron entry. The liver bypass is a consequence of the lymphatic route, not the reason for it.
2. D — SGLT1 is secondary active transport — it doesn't directly use ATP. Instead, Na⁺/K⁺ ATPase pumps on the basolateral membrane continuously pump Na⁺ out of the enterocyte, maintaining a low intracellular Na⁺ concentration. The resulting electrochemical gradient drives Na⁺ into the cell via SGLT1, and glucose is co-transported in the same direction.
3. A — Amino acids follow the same route as glucose: enterocyte → villus capillary → hepatic portal vein → liver (first pass) → hepatic vein → vena cava → systemic circulation. The hepatic portal vein is the key distinguishing feature from fat absorption.
4. C — The large intestine reabsorbs approximately 1.5L water per day. Diarrhoea accelerates transit time, leaving insufficient time for water reabsorption — large volumes of water pass through in liquid faeces. Drinking cannot keep pace because water must still be absorbed from the small intestine and this too may be impaired in conditions causing diarrhoea.
5. C — Fatty acids enter the enterocyte normally by simple diffusion (they are lipid-soluble and cross membranes directly without transport proteins). The problem occurs inside the enterocyte — without triglyceride assembly, chylomicrons cannot form, and without chylomicrons, fats cannot enter the lacteal. Fat would accumulate inside enterocytes or be lost.
At the macroscopic scale, the inner wall of the small intestine is folded into plicae circulares — large circular folds that triple the surface area compared to a smooth tube and slow chyme transit, increasing contact time between digestive contents and the absorptive surface.
At the tissue scale, each plica is covered in villi — finger-like projections approximately 0.5–1.6mm tall extending into the lumen. Each villus contains a capillary network and a lacteal. The villus structure increases surface area by approximately 10 times compared to the plica surface alone, and positions transport proteins close to the lumen where nutrients are present.
At the cellular scale, each enterocyte on the villus surface has its own surface covered in microvilli — tiny projections forming the brush border visible only by electron microscopy. The brush border increases absorptive surface area by approximately 20 times compared to a flat cell surface, and is the location of the transport proteins (SGLT1, GLUT2, amino acid transporters) responsible for moving nutrients into enterocytes.
The combined effect of all three levels of folding produces a total absorptive surface area of approximately 250m² — sufficient to absorb the full range of nutrients from a typical daily diet.
Glucose crosses the brush border into enterocytes via SGLT1 (sodium-glucose co-transport — secondary active transport driven by the Na⁺ gradient) and exits into the villus blood capillary via GLUT2 (facilitated diffusion). Capillaries drain into the hepatic portal vein, which carries glucose directly to the liver before it enters systemic circulation — the liver gets first pass and can store glucose as glycogen or allow it to pass through depending on blood glucose levels.
In contrast, fatty acids enter the enterocyte by simple diffusion (they are lipid-soluble and cross the membrane directly without transporters). Inside the enterocyte they are reassembled into triglycerides and packaged into chylomicrons by the Golgi apparatus. Chylomicrons are too large to enter blood capillaries and instead enter the lacteal — the lymph vessel in the villus core. They travel via the lymphatic system and thoracic duct into the left subclavian vein, entering systemic circulation near the heart and bypassing the liver entirely on first pass.
The large intestine reabsorbs approximately 1.3–1.8 litres of water per day. The mechanism is osmotic — Na⁺ ions are actively pumped from the colon lumen into the bloodstream by Na⁺/K⁺ ATPase pumps in the colon epithelium. This lowers the water potential of the blood and raises it in the colon lumen, causing water to move by osmosis from lumen to blood down its water potential gradient. Electrolytes (Cl⁻, K⁺) are also reabsorbed, further driving osmotic water movement.
When this process is disrupted — for example in diarrhoea caused by infection or gut motility disorders — intestinal contents pass through the colon too quickly for sufficient water reabsorption to occur. Large volumes of water remain in the faeces and are eliminated. This causes dehydration because more water is lost through the gut than can be replaced by drinking, particularly in severe cases where the infection also impairs small intestinal absorption.
Mystery solved. Tick when you've finished all activities and checked your answers.