Homeostasis
Every living cell operates within narrow chemical limits. Homeostasis is the set of mechanisms that keep internal conditions — blood glucose, body temperature, blood osmotic pressure — near a set point despite constant external change. Negative feedback loops, hormones that act as first messengers activating intracellular second messengers, and the kidney's remarkable countercurrent multiplier all work to maintain the dynamic equilibrium on which cell function depends. Plants face the same challenge through a different mechanism: guard cells and the hormone ABA integrate light, CO₂, and water-stress signals to regulate the stomatal pore.
Homeostasis principles & blood glucose
Principles of homeostasis
Homeostasis is the maintenance of a stable internal environment within narrow limits, despite continuous changes in the external environment and in the body's own metabolic activity. It is achieved through negative feedback loops that detect deviation from the set point and trigger corrective responses.
Detects the stimulus — a change in the internal condition (e.g. blood glucose rising above the set point). Sends a signal to the control centre. Examples: pancreatic β-cells that detect high blood glucose; osmoreceptors in the hypothalamus detecting high blood osmotic pressure.
Processes the signal and determines the appropriate response. Often the same structure as the receptor in endocrine systems (e.g. the pancreatic islets detect and respond), or a separate nervous structure (e.g. hypothalamus coordinates temperature regulation).
Carries out the corrective response. Brings the condition back toward the set point. Examples: liver cells converting glucose to glycogen; sweat glands increasing secretion; kidney collecting duct altering water reabsorption.
The response opposes the original change and returns conditions toward the set point. The result of the effector's action feeds back to reduce the signal — forming a closed loop. This is the basis of all homeostatic regulation.
Contrast: positive feedback amplifies the change (e.g. blood clotting, action potential depolarisation, oxytocin during childbirth) — not involved in homeostasis but can be tested in context.
Blood glucose regulation
Maintaining blood glucose in a narrow range (~4–6 mmol dm⁻³ fasting) is critical because glucose is the primary respiratory substrate for most cells, especially neurones which cannot switch to lipid respiration. Two antagonistic hormones from the islets of Langerhans regulate blood glucose by opposite mechanisms:
| Feature | Insulin | Glucagon |
|---|---|---|
| Cell of origin | Pancreatic β-cells | Pancreatic α-cells |
| Stimulus for release | High blood glucose (after a meal) | Low blood glucose (fasting, exercise) |
| Effect on blood glucose | Lowers | Raises |
| Primary target | Liver cells and muscle cells | Liver cells |
| Key liver processes activated | Glycogenesis (glucose → glycogen); reduced glycogenolysis | Glycogenolysis (glycogen → glucose); gluconeogenesis (non-carbohydrate → glucose) |
| Effect on glucose transporters | Increases glucose uptake into cells (more GLUT4 inserted into membranes) | Reduces cellular glucose uptake |
- Glycogenesis: glucose → glycogen (synthesis of glycogen). Activated by insulin.
- Glycogenolysis: glycogen → glucose (breakdown of glycogen). Activated by glucagon.
- Gluconeogenesis: non-carbohydrate precursors (e.g. amino acids, lactate, glycerol) → glucose. Activated by glucagon during prolonged fasting. Note: the prefix “neo” = new; this is new glucose from non-glucose sources.
All three terms are tested. Using them precisely — including the direction of each process — is essential in both MCQ and structured answers.
Cell signalling — glucagon and the cAMP pathway
The 9700 syllabus requires detailed knowledge of cell signalling using glucagon as the example. Glucagon is a protein hormone (first messenger) that cannot cross the hydrophobic plasma membrane — it must act through a cell-surface receptor to generate an intracellular second messenger.
- Blood glucose falls below the set point; α-cells in the islets of Langerhans of the pancreas detect this and secrete glucagon into the blood
- Glucagon (first messenger) travels in the blood to hepatocytes (liver cells)
- Glucagon binds to a complementary cell-surface receptor on the hepatocyte membrane, causing a conformational change in the receptor protein
- The conformational change activates a G-protein (GTP-binding protein) associated with the inner surface of the membrane
- The activated G-protein stimulates adenylyl cyclase (an enzyme in the membrane) to become active
- Adenylyl cyclase catalyses the conversion of ATP → cAMP (cyclic adenosine monophosphate) — the second messenger
- cAMP activates protein kinase A (PKA) inside the cell
- PKA initiates an enzyme cascade: it phosphorylates and activates further enzymes in sequence, each activating many more — this is signal amplification
- The final enzyme activated is glycogen phosphorylase, which catalyses glycogenolysis: glycogen → glucose-1-phosphate → glucose; blood glucose rises
- As blood glucose returns to the set point, α-cells reduce glucagon secretion — negative feedback
- Signal transduction without membrane crossing: glucagon is too large and polar to enter the cell. The receptor converts the extracellular signal into an intracellular one (cAMP) without the hormone needing to enter.
- Signal amplification: one glucagon molecule activates one receptor → one G-protein → one adenylyl cyclase molecule → many cAMP molecules → many PKA molecules → many enzyme molecules → enormous cellular response. Each step multiplies the signal.
Insulin (secreted by β-cells in response to high blood glucose) also acts through a cell-surface receptor and cannot cross the plasma membrane — but the 9700 syllabus requires the detailed cAMP signalling pathway only for glucagon. Insulin acts via a different intracellular mechanism (a receptor tyrosine kinase pathway) rather than the G-protein/adenylyl cyclase/cAMP route. For 9700, know that insulin:
- Is secreted by pancreatic β-cells when blood glucose is high
- Promotes glycogenesis in liver and muscle (glucose → glycogen)
- Increases uptake of glucose by muscle and adipose cells
- Inhibits glycogenolysis and gluconeogenesis in the liver
- Acts through a cell-surface receptor (protein hormone cannot enter the cell)
❌ Do not write “insulin uses cAMP as a second messenger” — this is incorrect for the 9700 syllabus. The official CED (LO 14.1.9) specifies glucagon as the hormone that uses the G-protein → adenylyl cyclase → cAMP → PKA → enzyme cascade pathway. Insulin uses a different receptor mechanism. Use glucagon for all cAMP signalling questions.
Type 1 and Type 2 diabetes mellitus
| Feature | Type 1 diabetes | Type 2 diabetes |
|---|---|---|
| Cause | Autoimmune destruction of pancreatic β-cells — little or no insulin is produced | Target cells develop insulin resistance — receptors lose sensitivity; insulin may still be produced but is ineffective |
| Onset | Typically childhood/early adulthood; rapid onset | Typically middle age or older; gradual onset |
| Risk factors | Genetic and autoimmune; not preventable by lifestyle | Obesity, physical inactivity, diet high in refined sugars, genetic predisposition; often preventable or manageable through lifestyle |
| Treatment | Insulin replacement (injected or pumped); carbohydrate monitoring | Lifestyle modification (diet, exercise, weight loss); oral medication (e.g. metformin); insulin injections in some cases |
| Blood glucose | Hyperglycaemia if untreated | Hyperglycaemia if uncontrolled |
Biosensors and blood glucose measurement
Managing diabetes requires regular measurement of blood glucose. The 9700 syllabus requires knowledge of both simple test strips and electronic biosensors:
Strips impregnated with glucose oxidase enzyme and a colour indicator. When blood (from a finger-prick) is applied, glucose oxidase catalyses the oxidation of glucose. The products react with the indicator to produce a colour change. The strip colour is compared against a reference chart to estimate glucose concentration — semi-quantitative and portable.
A biosensor combines a biological recognition element (glucose oxidase enzyme) with a transducer that converts the biological signal into a measurable electrical signal. Glucose oxidase oxidises glucose; the electrons released are detected by an electrode, producing a current proportional to glucose concentration. The glucometer converts this to a digital readout (mmol dm⁻³ or mg dl⁻¹).
Advantages over test strips: faster, more precise (quantitative), less user error.
Glucose normally does not appear in urine — it is completely reabsorbed in the PCT of the nephron (Topic 14.3). When blood glucose exceeds the renal threshold (~10 mmol dm⁻³), the PCT transporters are saturated and glucose appears in urine (glucosuria). Urine test strips detect this using the same glucose oxidase principle. However, urine testing gives only a historical reading, not a real-time blood glucose value — blood testing is more informative for management.
Which sequence correctly describes the response to a rise in blood glucose above the set point?
- A. α-cells detected rise → glucagon secreted → glycogenolysis in liver
- B. β-cells detected rise → insulin secreted → glycogenesis in liver and increased glucose uptake by cells
- C. β-cells detected rise → glucagon secreted → glycogenesis in liver
- D. α-cells detected rise → insulin secreted → gluconeogenesis in liver
Glucagon is a protein hormone that controls blood glucose concentration.
(a) Explain why glucagon must act via a cell-surface receptor rather than entering hepatocytes directly. [2]
(b) Describe the role of cAMP as a second messenger in the response of liver cells to glucagon. Include the role of G-protein, adenylyl cyclase, and signal amplification. [4]
(c) Explain how the concept of negative feedback applies to blood glucose regulation when blood glucose is low. [2]
(a) Why glucagon cannot enter the cell [2 marks]
- Glucagon is a large, polar protein molecule — it cannot diffuse through the hydrophobic lipid bilayer of the plasma membrane [1]
- It must bind to a complementary transmembrane receptor protein on the hepatocyte surface to transmit its signal into the cell [1]
(b) cAMP pathway in response to glucagon [4 marks]
- Glucagon binds to its cell-surface receptor on the hepatocyte, causing a conformational change; this activates a G-protein on the inner membrane surface [1]
- The G-protein activates adenylyl cyclase, which catalyses the conversion of ATP to cAMP (cyclic AMP) — cAMP is the second messenger [1]
- cAMP activates protein kinase A (PKA), which initiates an enzyme cascade by phosphorylating and activating further enzymes in sequence [1]
- Signal amplification occurs: each enzyme in the cascade activates many copies of the next enzyme, so one glucagon molecule produces an enormous cellular response; the final activated enzyme (glycogen phosphorylase) catalyses glycogenolysis — blood glucose rises [1]
(c) Negative feedback when blood glucose is low [2 marks]
- Low blood glucose is detected by α-cells in the pancreas → glucagon is secreted → glycogenolysis in the liver raises blood glucose back toward the set point [1]
- As blood glucose rises to the set point, the stimulus for α-cell secretion is reduced, so glucagon secretion decreases — the response opposes and corrects the original change (negative feedback) [1]
Kidney & osmoregulation
The kidney serves two closely linked functions: excretion (removal of nitrogenous waste products, especially urea) and osmoregulation (controlling the water potential of the blood). Each human kidney contains approximately one million nephrons — the functional units that produce urine through a combination of filtration, reabsorption, and secretion.
Nephron structure
| Structure | Location | Function |
|---|---|---|
| Glomerulus | Cortex | Knot of capillaries; high hydrostatic pressure forces fluid out of blood into Bowman’s capsule (ultrafiltration) |
| Bowman’s capsule | Cortex | Cup-shaped structure surrounding the glomerulus; receives the filtrate; start of nephron tubule |
| Proximal convoluted tubule (PCT) | Cortex | Major site of selective reabsorption — glucose, amino acids, most water, ions; epithelium has microvilli (brush border) and many mitochondria |
| Loop of Henle | Medulla (descending into and ascending out) | Countercurrent multiplier — establishes osmotic gradient in the medulla that allows variable water reabsorption from the collecting duct |
| Distal convoluted tubule (DCT) | Cortex | Fine adjustment of ionic composition and pH; responds to aldosterone (Na⁺ reabsorption) and ADH |
| Collecting duct | Medulla | Carries concentrated urine toward the renal pelvis; permeability to water controlled by ADH via aquaporins |
Ultrafiltration
Ultrafiltration forces small molecules from the blood into the Bowman’s capsule under high hydrostatic pressure:
- Blood enters the glomerulus through the wide afferent arteriole and leaves through the narrower efferent arteriole — the size difference maintains high hydrostatic pressure inside the glomerular capillaries
- High hydrostatic pressure forces fluid through two filtration barriers: (a) the fenestrated (porous) endothelium of the capillary wall; (b) the basement membrane (acts as a molecular sieve); (c) the podocytes of the Bowman’s capsule, which have filtration slits between their processes
- Small molecules pass through: water, glucose, amino acids, urea, ions, creatinine
- Large molecules are retained in the blood: proteins, red blood cells, platelets (too large to pass through filtration slits)
- The resulting fluid in the Bowman’s capsule is glomerular filtrate — essentially plasma minus proteins
The human glomerular filtration rate (GFR) is approximately 180 litres of filtrate per day. Since urine output is only ~1.5 litres per day, around 99% of the filtrate is reabsorbed — mostly in the PCT, with variable recovery in the collecting duct.
Selective reabsorption in the PCT
The proximal convoluted tubule (PCT) reabsorbs ~65–70% of the filtrate. Its epithelium has specialised features for rapid, large-scale reabsorption:
Reabsorbed entirely by co-transport: Na⁺ ions are pumped out of the cell into the blood by the Na⁺/K⁺ ATPase (active transport, requires ATP); this creates a low Na⁺ concentration inside the cell; Na⁺ diffuses back in from the tubule fluid via co-transporter proteins, carrying glucose or amino acids with it (facilitated diffusion driven by the Na⁺ gradient). Glucose then exits by facilitated diffusion into the blood.
As solutes (glucose, Na⁺) are reabsorbed, the water potential of the tubule fluid falls; water follows by osmosis through aquaporin channels in the PCT epithelium. This “obligatory” water reabsorption accounts for ~65% of filtered water and does not depend on ADH.
Urea is not reabsorbed by active transport. As water is reabsorbed, urea concentration in the tubule fluid rises. Urea diffuses passively down its concentration gradient back into the blood in the PCT. The remainder passes through the Loop of Henle and collecting duct, and is excreted in urine.
- Microvilli (brush border) on the apical surface — increase surface area ~30-fold for reabsorption
- Many mitochondria in the cells — provide ATP for Na⁺/K⁺ ATPase pumps
- Many co-transporter and carrier proteins in the cell membrane
- Tight junctions prevent leakage back into the tubule
Loop of Henle — the countercurrent multiplier
The loop of Henle is the key to variable urine concentration. It establishes an osmotic gradient in the medullary tissue fluid, from cortex (lower concentration) to the deepest medulla (very high concentration). This gradient allows the collecting duct to reabsorb more or less water depending on ADH levels.
Descending limb (thin, permeable to water, impermeable to NaCl):
- Fluid entering the descending limb from the PCT has a low osmolarity (~300 mosmol L⁻¹)
- As fluid descends into the increasingly hypertonic medullary tissue fluid, water leaves by osmosis and NaCl is not pumped out — the tubular fluid becomes progressively more concentrated as it descends
- Fluid at the hairpin bend reaches maximum concentration (~1200 mosmol L⁻¹)
Ascending limb (thick wall, impermeable to water, actively pumps out NaCl):
- As fluid ascends, NaCl is actively transported out into the medullary tissue fluid using ATP (the ascending limb is impermeable to water, so water cannot follow)
- The active NaCl transport progressively raises the osmolarity of the medullary tissue fluid
- Fluid in the ascending limb becomes more dilute as it approaches the DCT (~100 mosmol L⁻¹)
Result: a steep osmotic gradient in the medulla; deepest medulla has extremely high NaCl concentration. This gradient determines how concentrated the urine can be when the collecting duct runs through the medulla.
Animals living in arid environments (e.g. desert rodents like kangaroo rats) have very long loops of Henle, producing extremely concentrated urine. Animals with abundant water access (e.g. freshwater fish) have shorter loops or none. Humans have loops of intermediate length. This is a classic adaptation-to-environment example linking kidney anatomy to habitat.
ADH and aquaporins — variable water reabsorption
ADH (antidiuretic hormone; also called vasopressin) is a small peptide hormone produced in the hypothalamus and released from the posterior pituitary gland. It controls the permeability of the collecting duct to water:
- When blood osmotic pressure rises (dehydration), osmoreceptors in the hypothalamus detect the change
- The hypothalamus signals the posterior pituitary to release more ADH into the blood
- ADH travels in the blood to the collecting duct cells
- ADH binds to cell surface receptors, activating a signalling cascade (using cAMP — same second messenger principle as insulin)
- Intracellular vesicles containing aquaporin channel proteins (AQP2) are inserted into the apical plasma membrane of collecting duct cells
- With more aquaporins, the collecting duct becomes more permeable to water; water moves by osmosis from the collecting duct fluid into the hypertonic medullary tissue fluid, then into blood capillaries (vasa recta)
- More concentrated urine is produced; smaller volume of urine is excreted
- Blood osmotic pressure falls back toward normal; ADH secretion reduces (negative feedback)
Blood osmotic pressure high → hypothalamus detects → more ADH released → more aquaporins inserted in collecting duct → more water reabsorbed → concentrated urine (small volume, high urea, high NaCl) → blood osmotic pressure falls back to normal.
Blood osmotic pressure low → less ADH released → fewer aquaporins in collecting duct → less water reabsorbed → dilute urine (large volume, low urea concentration) → blood osmotic pressure rises back toward normal.
Aquaporins are transmembrane channel proteins that allow water molecules to move rapidly across the membrane without carrying ions. Their insertion into the collecting duct membrane (under ADH stimulation) dramatically increases water permeability. Without aquaporins, water crosses membranes slowly; with them, water reabsorption is fast and efficient. The number of aquaporins in the membrane is directly regulated by ADH concentration — this is the molecular basis of variable urine concentration.
A student runs a marathon and becomes significantly dehydrated. Which correctly describes the expected changes in ADH secretion and urine output?
- A. ADH decreases; urine volume increases; urine becomes more dilute
- B. ADH increases; urine volume decreases; urine becomes more concentrated
- C. ADH increases; urine volume increases; urine becomes more dilute
- D. ADH decreases; urine volume decreases; urine becomes more concentrated
The loop of Henle and the collecting duct together determine the final concentration of urine.
(a) Describe the role of each limb of the loop of Henle in establishing a medullary osmotic gradient. [4]
(b) Explain how ADH increases water reabsorption from the collecting duct, at the cellular level. [3]
(c) Explain why glucose does not normally appear in urine, and under what condition it might. [2]
(a) Loop of Henle: descending + ascending [4 marks]
- Descending limb: permeable to water, not NaCl; as fluid descends into hypertonic medullary tissue, water leaves by osmosis; tubule fluid becomes increasingly concentrated [2]
- Ascending limb: impermeable to water; NaCl is actively transported out into medullary tissue fluid; tubule fluid becomes more dilute as it ascends; the active NaCl transport builds up the high osmolarity in the medulla — the countercurrent multiplier effect [2]
(b) ADH mechanism at cellular level [3 marks]
- ADH binds to receptor proteins on collecting duct cells, activating a signalling cascade involving cAMP as a second messenger [1]
- Vesicles containing aquaporin channel proteins (AQP2) are inserted into the apical membrane of the collecting duct cells [1]
- Aquaporins increase membrane permeability to water; water moves by osmosis from the dilute collecting duct fluid into the concentrated medullary tissue fluid, and then into blood capillaries; concentrated, low-volume urine results [1]
(c) Glucose and the renal threshold [2 marks]
- Glucose is completely reabsorbed in the PCT by co-transport with Na⁺ ions — under normal blood glucose concentrations, all filtered glucose is recovered before the end of the PCT [1]
- If blood glucose rises above the renal threshold (~10 mmol dm⁻³), the carrier proteins become saturated and cannot reabsorb all the filtered glucose; the excess passes into urine as glucosuria (seen in uncontrolled diabetes mellitus) [1]
Plant homeostasis — stomatal regulation
Plants face a fundamental conflict: stomata must be open for CO₂ to diffuse in for photosynthesis, but every open pore loses water vapour through transpiration (Topic 7). Plant homeostasis resolves this conflict through guard cell regulation — the daily rhythm of stomatal opening and closing, and the rapid stress response mediated by abscisic acid (ABA) under water deficit.
Daily rhythm of stomatal opening and closing
Stomata follow a daily (circadian) rhythm tied to light and CO₂ availability:
| Condition | Stomatal response | Reason |
|---|---|---|
| High light intensity (daytime) | Open | Photosynthesis requires CO₂; light drives the K⁺ pump mechanism; CO₂ inside the leaf is consumed by photosynthesis, so [CO₂] inside leaf falls |
| Low CO₂ inside leaf | Open | Low CO₂ is a signal that photosynthesis is occurring and more CO₂ is needed |
| Darkness (night) | Closed | No photosynthesis; CO₂ accumulates inside leaf (from respiration); light-driven K⁺ pump stops; conserves water |
| High CO₂ inside leaf | Closed | High [CO₂] signals that photosynthesis rate is low or respiration is high; stomatal closure conserves water |
| Water stress (wilting) | Closed | ABA mechanism (see below) |
Mechanism of stomatal opening
- Light is absorbed by guard cell chloroplasts; this drives ATP synthesis by photophosphorylation (Topic 13)
- ATP powers a proton pump (H⁺-ATPase) in the guard cell plasma membrane, pumping H⁺ out of the guard cell into the surrounding cells
- This creates a negative electrical charge inside the guard cell (the cell becomes more negative)
- The electrochemical gradient drives K⁺ ions into the guard cell through K⁺ channels
- The influx of K⁺ (an osmotically active solute) lowers the water potential of the guard cell
- Water enters the guard cell by osmosis from surrounding cells
- Guard cells become turgid; their asymmetric cell wall structure (thicker on the inner side facing the pore) causes them to bow outward — opening the stomatal pore
Mechanism of stomatal closing
- In darkness, the proton pump stops (no ATP from photophosphorylation)
- K⁺ channels close and K⁺ ions leave the guard cells (K⁺ efflux)
- Water potential of guard cells rises
- Water leaves guard cells by osmosis
- Guard cells become flaccid; the pore narrows and closes
Abscisic acid (ABA) — rapid stomatal closure under water stress
ABA (abscisic acid) is a plant hormone synthesised primarily in leaf mesophyll cells and roots in response to water deficit. It triggers rapid stomatal closure within minutes, overriding the circadian rhythm:
- Water deficit in the leaf → ABA concentration rises in the mesophyll and is transported to guard cells
- ABA binds to receptors on the guard cell plasma membrane and inside the guard cell
- ABA signalling activates channels that allow Ca²⁺ ions to enter the cytoplasm of guard cells from vacuoles and from outside; Ca²⁺ acts as a second messenger
- Elevated Ca²⁺ inhibits the H⁺-ATPase (proton pump) — K⁺ influx stops
- Ca²⁺ also activates channels that allow K⁺ to leave the guard cells (K⁺ efflux)
- K⁺ leaving raises the water potential inside the guard cells; water leaves by osmosis
- Guard cells become flaccid; the stomata close, reducing water loss by transpiration
- Produced by mesophyll cells in water-stressed leaves
- Rapidly (minutes) closes stomata by triggering K⁺ efflux
- Uses Ca²⁺ as an intracellular second messenger
- Inhibits the proton pump, preventing K⁺ influx
- Overrides the light-induced opening signal during water stress
Closing stomata reduces water loss (good) but also restricts CO₂ entry — slowing photosynthesis. Plants under prolonged water stress therefore grow more slowly. ABA-induced stomatal closure is an emergency response that prioritises survival over growth. When water availability is restored, ABA levels fall and stomata reopen.
Which of the following correctly describes the role of K⁺ ions in stomatal opening?
- A. K⁺ enters guard cells, raising their water potential, causing water to leave by osmosis
- B. K⁺ enters guard cells, lowering their water potential, causing water to enter by osmosis, making cells turgid
- C. K⁺ leaves guard cells, lowering their water potential, causing water to enter by osmosis
- D. K⁺ enters guard cells, increasing their pH, activating photosynthesis
Topic 14 Practice — Comprehensive
Mixed practice across all four homeostasis sub-topics.
Which of the following is an example of negative feedback in mammalian homeostasis?
- A. Oxytocin causing stronger uterine contractions during childbirth, which stimulates more oxytocin release
- B. A rise in blood glucose stimulating insulin secretion, which causes blood glucose to fall back toward the set point
- C. Blood clotting factors activating each other in a cascade after vessel damage
- D. Action potential depolarisation opening more Na⁺ channels, accelerating further depolarisation
A patient is found to have protein molecules in their urine. This finding most likely indicates damage to which structure of the nephron?
- A. The loop of Henle
- B. The proximal convoluted tubule
- C. The glomerular filtration barrier (glomerulus / basement membrane / podocytes)
- D. The collecting duct
Diabetes mellitus affects millions of people globally.
(a) Distinguish between Type 1 and Type 2 diabetes, including their causes and how each can be treated. [4]
(b) A person with uncontrolled Type 1 diabetes has consistently high blood glucose. Explain why glucose appears in their urine, using your knowledge of nephron function. [2]
(c) The biosensor used to monitor blood glucose contains glucose oxidase. Explain the principle by which this biosensor works. [2]
(a) Type 1 vs Type 2 [4 marks]
- Type 1: autoimmune destruction of pancreatic β-cells; little/no insulin produced; requires insulin injections or pump for treatment [2]
- Type 2: target cells become resistant to insulin (receptor sensitivity decreases); insulin may still be produced; treated by lifestyle changes, oral medications, or insulin injections in some cases [2]
(b) Glucosuria mechanism [2 marks]
- Normally, all glucose filtered at the glomerulus is reabsorbed in the PCT by co-transport with Na⁺ ions; however the carrier proteins become saturated above the renal threshold (~10 mmol dm⁻³) [1]
- In uncontrolled Type 1 diabetes, blood glucose is persistently above the renal threshold; the PCT cannot reabsorb all the filtered glucose, so excess glucose remains in the tubule fluid and is excreted in urine [1]
(c) Biosensor principle [2 marks]
- Glucose oxidase catalyses the oxidation of glucose in the blood sample; this reaction releases electrons [1]
- A transducer (electrode) detects the electrons, generating an electrical current proportional to the glucose concentration; the glucometer converts this to a digital glucose reading [1]
During a drought, a plant rapidly closes its stomata within minutes.
(a) Name the hormone responsible for this rapid closure. [1]
(b) Describe the mechanism by which this hormone causes stomatal closure. [4]
(c) Explain the physiological cost to the plant of prolonged stomatal closure. [2]
(d) Explain why stomata open in response to light, referring to the role of ATP. [1]
(a) Hormone [1 mark]
- Abscisic acid (ABA) [1]
(b) ABA closure mechanism [4 marks]
- ABA binds to receptors on guard cell membranes, triggering signalling cascade [1]
- Ca²⁺ ions enter the cytoplasm of guard cells (second messenger), inhibiting the proton pump (H⁺-ATPase) and stopping K⁺ influx [1]
- Ca²⁺ also activates K⁺ efflux channels; K⁺ leaves guard cells [1]
- Guard cell water potential rises; water leaves by osmosis; cells become flaccid and the stomatal pore closes [1]
(c) Cost of prolonged closure [2 marks]
- CO₂ cannot enter through closed stomata, limiting the supply of substrate for RuBisCO in the Calvin cycle [1]
- Photosynthesis rate falls, reducing organic molecule production and ultimately restricting plant growth and biomass accumulation [1]
(d) Light drives stomatal opening via ATP [1 mark]
- Light is absorbed by guard cell chloroplasts, driving photophosphorylation to produce ATP; ATP powers the H⁺-ATPase proton pump, which creates the electrochemical gradient driving K⁺ influx and turgidity [1]
Topic 14 — Common Mistakes
- 🔏Swapping α-cells and β-cellsThis is one of the most frequent exam errors in all of biology. Memorise: β-cells make insulin (blood glucose too high → lower it); α-cells make glucagon (blood glucose too low → raise it). β looks like a B for “blood-glucose lowering”.
- 🧰Confusing glycogenesis, glycogenolysis, gluconeogenesisAll three are liver processes: glycogenesis = making glycogen (glucose → glycogen; insulin); glycogenolysis = breaking glycogen (glycogen → glucose; glucagon); gluconeogenesis = new glucose from non-carbohydrates (e.g. amino acids, lactate; glucagon). The suffix tells you the direction; “neo” = new synthesis from scratch.
- 🧰Saying K⁺ influx raises guard cell water potentialReversed. K⁺ is a solute — its entry lowers water potential (more solutes = lower water potential). Lower water potential draws water IN by osmosis, causing turgidity and opening. If you write “K⁺ raises water potential”, the rest of the answer unravels.
- 🖤Saying glucose is reabsorbed by osmosis in the PCTGlucose is reabsorbed by co-transport (secondary active transport), driven by the Na⁺ gradient established by Na⁺/K⁺-ATPase. This requires ATP indirectly. Osmosis is the mechanism for water reabsorption, not glucose. This is a commonly confused mechanism.
- 💤Saying ADH is produced by the pituitary glandImprecise. ADH is produced in the hypothalamus (by hypothalamic neurones) and stored and released from the posterior pituitary. Saying “the pituitary produces ADH” misidentifies the site of synthesis and loses the mark.
- 🖤Describing the loop of Henle as "reabsorbing water in the ascending limb"The ascending limb is impermeable to water — that is the whole point. It actively pumps NaCl OUT while keeping water IN. Water is only reabsorbed in the descending limb (passively, by osmosis). The asymmetry between the two limbs is what builds the medullary gradient.
- 🌿Saying ABA directly opens K⁺ channels for efflux without mentioning Ca²⁺The mechanism involves Ca²⁺ as an intermediate second messenger: ABA → Ca²⁺ influx → Ca²⁺ inhibits H⁺-ATPase AND activates K⁺ efflux channels. Skipping Ca²⁺ loses the mechanism mark. The Ca²⁺ step is required.
- 🥜Saying "insulin enters liver cells directly"Insulin is a large protein hormone and cannot cross the plasma membrane. It binds to a surface receptor (transmembrane glycoprotein) and signals via cAMP as a second messenger inside the cell. Never say a protein hormone enters the target cell.
- 💡Confusing Type 1 and Type 2 diabetes mechanismsType 1: β-cells destroyed by autoimmune response → no insulin produced. Type 2: insulin is produced but target cells do not respond (insulin resistance). The treatment difference follows directly: Type 1 always needs insulin replacement; Type 2 may be managed without insulin using lifestyle changes and oral medications. Don't swap the mechanisms.
- 🔍Saying ultrafiltration is a selective processUltrafiltration is not selective — it is a size-based (non-selective) filtration driven by hydrostatic pressure. All small molecules pass through regardless of whether they are useful or waste. Selectivity comes later, in the PCT through reabsorption. Mixing up filtration (physical) and reabsorption (enzymatic/transport) is a common essay error.
- 😏Saying aquaporins are "inserted into guard cell membranes" when answering about stomatal openingAquaporins in the collecting duct are an ADH/kidney story, not a stomatal opening story. Stomatal opening uses K⁺ influx and osmosis, not aquaporin insertion. Don't cross-contaminate the two homeostatic mechanisms.
Topic 14 is one of the most mark-rich A Level topics — it contains multiple high-frequency essay targets. Highest-yield items: β-cells/insulin vs α-cells/glucagon with correct effects, glycogenesis vs glycogenolysis vs gluconeogenesis directions, cAMP as second messenger for glucagon (G-protein → adenylyl cyclase → cAMP → PKA → enzyme cascade → glycogenolysis), not insulin, Type 1 vs Type 2 distinction, ultrafiltration barrier components, PCT co-transport for glucose (NOT osmosis), loop of Henle asymmetry (descending permeable to water / ascending impermeable + active NaCl pump), ADH produced in hypothalamus / released from posterior pituitary / inserts aquaporins in collecting duct, stomatal opening via H⁺-ATPase → K⁺ influx → osmosis → turgidity, ABA → Ca²⁺ → K⁺ efflux → stomatal closure. Synoptic links: Topic 4 (osmosis, water potential, co-transport), Topic 7 (stomata and transpiration), Topic 12B (gluconeogenesis from amino acids needs deamination → Topic 14 excretion), Topic 13 (ATP in guard cells for proton pump).