BIOSCI107 · Biology for Biomedical Science: Cellular Processes and Development
Membrane Transport & Epithelial Function
Topic 4 (exam Section B) is the first of the exam-only topics: how molecules cross membranes. It contrasts passive and active transport (channels vs carriers, the electrogenic Na⁺/K⁺-ATPase, osmosis and aquaporins), then applies it to epithelia — glucose absorption via SGLT/GLUT and the renal threshold, and chloride secretion via NKCC and CFTR, with the clinical twists of cholera and cystic fibrosis (where CFTR is a phosphorylation- and ATP-gated channel, not a pump). Examined in the 40% final exam as paper Teleform MCQ.
What this chapter covers
- 01Transport axes: non-mediated vs mediated (protein), and passive (down gradient, no energy) vs active (against gradient, energy)
- 02Simple diffusion of nonpolar molecules (O₂, CO₂, steroids, fat-soluble vitamins) straight through the bilayer
- 03Ion channels (fast, selective, gated) vs carriers (slower, enzyme-like: specificity, competition, saturation/transport maximum)
- 04Primary active transport: the Na⁺/K⁺-ATPase (3 Na⁺ out : 2 K⁺ in, electrogenic, ~30% of cell energy)
- 05Secondary active transport: symporters (Na⁺-glucose) and antiporters (Na⁺/Ca²⁺) powered by the Na⁺ gradient
- 06Osmosis and water permeability Pw = Pd (bilayer) + Pf (aquaporins)
- 07Epithelial glucose absorption: apical SGLT (secondary active) → basolateral GLUT (facilitated); the renal threshold = SGLT transport maximum
- 08Chloride secretion: basolateral NKCC accumulates Cl⁻ → apical CFTR channel; cholera (over-activation → secretory diarrhoea) and cystic fibrosis (loss of function)
Tracing glucose across an intestinal epithelial cell
- +1Apical uptake against the gradient. The apical (lumen-facing) membrane has SGLT, a Na⁺–glucose symporter. It uses the inward Na⁺ electrochemical gradient to drag glucose INTO the cell even though glucose is being concentrated against its own gradient — this is secondary active transport. [+1]
- +1What powers it. SGLT does not hydrolyse ATP itself; it rides the Na⁺ gradient. That gradient is built by the basolateral Na⁺/K⁺-ATPase (3 Na⁺ out : 2 K⁺ in, primary active), which keeps intracellular Na⁺ low so Na⁺ keeps flowing in through SGLT. This is the 'active' step, one membrane removed from the glucose. [+1]
- +1Basolateral exit. Glucose has now accumulated inside the cell, so it leaves down its gradient through GLUT (a facilitated-diffusion carrier) on the basolateral membrane into the interstitial fluid and blood. No energy needed here. [+1]
- +1Renal threshold. In the kidney the same SGLT reabsorbs filtered glucose. The renal threshold is the plasma glucose concentration at which SGLT reaches its transport maximum (saturation) — above it, excess glucose can no longer be reabsorbed and spills into the urine. [+1]
Key terms
- Na⁺/K⁺-ATPase
- The primary active transporter that pumps 3 Na⁺ out and 2 K⁺ in per ATP, keeping intracellular Na⁺ low and K⁺ high. It is electrogenic (net positive charge exported) and consumes about 30% of the cell's energy. The Na⁺ gradient it builds powers secondary active transport.
- Secondary active transport
- Movement of a solute against its gradient powered indirectly by the Na⁺ gradient rather than by ATP directly — via symporters (e.g. Na⁺-glucose SGLT) or antiporters (e.g. Na⁺/Ca²⁺). It depends on the Na⁺/K⁺-ATPase to maintain that gradient.
- SGLT / GLUT
- The two-carrier system for epithelial glucose transport: apical SGLT is a Na⁺-glucose symporter that concentrates glucose in the cell (secondary active), and basolateral GLUT is a facilitated-diffusion carrier that lets glucose exit down its gradient to the blood.
- Renal threshold (for glucose)
- The plasma glucose concentration at which the kidney's SGLT transporters reach their transport maximum (saturate). Above this level, filtered glucose can no longer be fully reabsorbed and spills into the urine (glucosuria) — as in uncontrolled diabetes.
- CFTR
- An apical chloride channel gated open by phosphorylation of its R domain plus ATP binding at its nucleotide-binding domains — a channel, not a primary active pump. Cholera toxin over-activates it (via cAMP) causing secretory diarrhoea; loss of function causes cystic fibrosis.
- Aquaporin
- A water channel that raises a membrane's water permeability. Total water permeability Pw = Pd (diffusion through the bilayer) + Pf (through aquaporins); Pf is mercury-sensitive and temperature-independent, and the aquaporin isoforms present set a cell's water permeability.
Membrane Transport & Epithelial Function FAQ
Is CFTR a pump or a channel?
A channel — this is the exam's favourite catch. CFTR is a chloride channel gated open by phosphorylation of its R domain plus ATP binding at its nucleotide-binding domains. It does not hydrolyse ATP to pump Cl⁻ against a gradient the way a primary active pump would; Cl⁻ moves through it down its electrochemical gradient once the gate is open. The ATP here is a gating signal, not the energy source for uphill transport.
Why does cholera cause such severe diarrhoea, and why does oral rehydration work?
Cholera toxin locks the cAMP pathway on, over-activating the apical CFTR chloride channel. Cl⁻ pours into the gut lumen, Na⁺ follows paracellularly to balance charge, and water follows osmotically — producing massive secretory diarrhoea. Oral rehydration therapy works because SGLT is untouched: giving Na⁺ AND glucose together drives SGLT-mediated uptake of Na⁺ and glucose, and water follows that back into the body, out-competing the secretory loss.
How is secondary active transport 'active' if it doesn't use ATP directly?
It moves a solute against its gradient, which is the definition of active transport, but it borrows the energy stored in the Na⁺ gradient rather than hydrolysing ATP itself. That Na⁺ gradient was built by the Na⁺/K⁺-ATPase using ATP, so ATP is still ultimately the source — just one membrane step removed. Inhibit the pump and secondary active transport stops as the gradient dissipates.
Can AI help me with membrane transport in BIOSCI 107?
Yes, for study. Sia can trace SGLT/GLUT glucose absorption, explain the CFTR channel-not-pump point, and drill passive-vs-active classification. Use it to prepare for the final exam — it does not sit the exam for you, and the exam is an AI-free lane under the course's academic-integrity policy. Confirm the rules on Canvas.
Exam move
Build the two-by-two you'll be graded on — mediated vs non-mediated crossed with passive vs active — and be able to slot any example into it (O₂ = non-mediated passive; GLUT glucose = mediated passive; Na⁺/K⁺-ATPase = primary active; SGLT = secondary active). Learn the Na⁺/K⁺-ATPase numbers (3 out : 2 in, electrogenic) because it powers everything downstream. For the epithelial half, draw a polarised cell and place the transporters correctly (apical SGLT and CFTR; basolateral GLUT, NKCC and the Na⁺/K⁺-ATPase), and be able to say which single step actually consumes ATP. Nail the three clinical hooks the exam reuses — renal threshold (SGLT saturation), cholera (CFTR over-activation → oral rehydration), and cystic fibrosis (CFTR loss of function) — and the channel-not-pump identity of CFTR. This is exam material (Topic 4, Section B); confirm the exam date and Teleform format on Canvas.
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