OCR A Level Biology A: Hormonal communication and blood glucose control (H420) – Revision Notes

These notes condense topic 5.1.4, Hormonal communication, from OCR A Level Biology A (H420), Version 4.1 (April 2026), for first assessment in 2025. For full explanations and worked examples, read the study guide, then test yourself with the practice set. The OCR A Level Biology hub and checklist show where this fits, and the free diagnostics help you find weak spots. For the microscopy and drawing skills behind outcome (c), see the practical skills revision notes.

Key terms

Term	Meaning
Hormone	Chemical messenger secreted into the blood by an endocrine gland
Endocrine gland	Ductless gland; its secretion enters blood capillaries
Target cell	Cell with receptors complementary to a particular hormone
Exocrine gland	Gland that secretes through a duct
Islets of Langerhans	Clusters of endocrine cells in the pancreas
Negative feedback	A response that reverses a change and so restores the set point
Glycogenesis	Glucose to glycogen
Glycogenolysis	Glycogen to glucose
Gluconeogenesis	Glucose made from non-carbohydrates (amino acids, glycerol)
Second messenger	Molecule inside the cell, such as cAMP, made after a hormone binds its surface receptor

5.1.4(a) Endocrine communication

Three stages: secretion into the blood, transport by the blood to all tissues, detection by target cells with specific receptors.

• Water-soluble hormones (insulin, glucagon, adrenaline): receptor on the cell surface membrane, signal passed on inside the cell.
• Steroid hormones (cortisol, aldosterone): lipid-soluble, enter the cell, receptor inside, change gene transcription.
• Compared with nerves: slower, longer-lasting, widespread.

5.1.4(b) Adrenal glands

Position: one above each kidney. Two regions.

Region	Hormones	Functions to learn
Cortex (outer)	Mineralocorticoids (aldosterone)	Sodium retention and potassium loss at the kidney; maintains blood volume and pressure
Cortex (outer)	Glucocorticoids (cortisol)	Raise blood glucose, reduce inflammation, long-term stress response
Medulla (inner)	Adrenaline, noradrenaline	Fight or flight: faster heart rate, wider airways, glycogenolysis, blood diverted to muscle

The medulla is controlled by sympathetic neurones. Adrenaline raises blood glucose, so it opposes insulin.

5.1.4(c) Pancreas histology

Feature	Exocrine tissue (acini)	Endocrine tissue (islets)
Staining	Darker	Paler
Arrangement	Clusters around small ducts	Scattered patches with no ducts
Product	Digestive enzymes, which travel along ducts	Hormones, which enter capillaries
Cells	Acinar cells	Alpha (glucagon) and beta (insulin) cells

With a routine stain you cannot separate alpha from beta cells.

Method in steps: labelled drawing

1. Low power: tissue plan, outlines only.
2. High power: a few cells, with nuclei.
3. Sharp pencil, continuous lines, no shading, large drawing.
4. Ruled label lines, not crossing.
5. Title, magnification, scale bar.

Worked reminder. A drawing of an islet is 45 mm across. The real islet is 150 µm across. Magnification = 45 mm ÷ 0.150 mm = ×300. Rearranged: actual size = drawing size ÷ magnification.

5.1.4(d) Regulating blood glucose

	After a meal (glucose high)	After fasting or exercise (glucose low)
Cells that detect	Beta cells	Alpha cells
Hormone	Insulin	Glucagon
Liver	Glycogenesis	Glycogenolysis and gluconeogenesis
Other effects	More glucose uptake by muscle and fat; more respiration	Fat and protein used more
Result	Glucose falls	Glucose rises

Negative feedback: change, detection, hormone, response that reverses the change, stimulus shrinks, hormone release falls. The liver is well placed because the hepatic portal vein brings blood from the gut straight to it.

Glucagon and adrenaline signalling in outline

1. Hormone (first messenger) binds the surface receptor.
2. Adenylyl cyclase is activated.
3. ATP is converted to cyclic AMP (second messenger).
4. cAMP starts an enzyme cascade that breaks down glycogen.
5. Glucose leaves the liver cell and enters the blood.

Insulin secretion: the beta cell sequence

1. Glucose enters the beta cell by facilitated diffusion.
2. Respiration makes more ATP.
3. ATP closes potassium ion channels.
4. Membrane depolarises.
5. Voltage-gated calcium ion channels open and calcium ions enter.
6. Insulin vesicles fuse with the membrane: exocytosis.

Predictions: a drug that closes the potassium channels causes secretion at low glucose; a calcium channel blocker prevents secretion at high glucose; a drug that holds potassium channels open prevents depolarisation, so no insulin is released.

Worked reminder. Fasting glucose is 11.0 mmol dm⁻³, then falls to 6.6 after treatment. Percentage fall = (11.0 − 6.6) ÷ 11.0 × 100 = 40%.

5.1.4(e) Type 1 and Type 2

	Type 1	Type 2
Cause	Autoimmune destruction of beta cells	Target cells respond poorly to insulin; beta cells may fail later
Insulin	Little or none	Normal or high at first
Risk	Genetic and environmental factors	Obesity, inactivity, age, family history, ethnic background
Treatment	Insulin (injections or pump), monitoring, carbohydrate management	Diet, weight loss, exercise; metformin; sulfonylureas; sometimes insulin

Type 1 is the specification’s example of medical technology regulating a hormonal system: glucose sensors with insulin pumps, which can adjust the dose automatically.

Drug mechanisms: metformin lowers glucose output by the liver and improves sensitivity. Sulfonylureas close beta cell potassium channels and so stimulate insulin release.

5.1.4(f) Potential treatments

GM bacteria make human insulin

1. Get the insulin gene (no introns, for example from mRNA).
2. Cut gene and plasmid with the same restriction enzyme.
3. Join with DNA ligase.
4. Put the recombinant plasmid into bacteria and use a marker to find them.
5. Culture in a fermenter.
6. Extract and purify.

Advantages over animal insulin: human sequence, so a lower chance of immune reaction; plentiful supply; fewer ethical and religious issues.

Stem cells

Idea: turn stem cells into beta cells and transplant them. Issues: rejection and the need for immunosuppression, possible renewed autoimmune attack in Type 1, ethical objections to embryonic cells, tumour risk, and limited evidence so far.

Quick self-test

1. State the three stages of endocrine communication.
2. Name the hormones released by the adrenal medulla.
3. Name one hormone from the adrenal cortex and state its function.
4. A photomicrograph of an islet is printed at ×50. The islet measures 15 mm across on the print. Calculate its actual width in micrometres.
5. Name the process by which the liver forms glycogen from glucose.
6. Describe what happens to potassium channels in a beta cell when blood glucose rises.
7. In an illustrative exercise, an insulin dose is set at 1 unit per 12 g of carbohydrate. How many units match a meal containing 78 g of carbohydrate? (Real doses are set by clinicians.)
8. Blood glucose falls from 12.4 to 7.0 mmol dm⁻³ over 90 minutes. Calculate the mean rate of fall per hour.
9. Blood glucose is 9.6 mmol dm⁻³ before a drug and 5.2 after. Calculate the percentage change.
10. State why bacteria are given a gene without introns.

Answers

1. Secretion into the blood, transport by the blood, detection by target cells.
2. Adrenaline and noradrenaline.
3. Cortisol raises blood glucose (or aldosterone increases sodium reabsorption in the kidney).
4. 15 ÷ 50 = 0.30 mm = 300 µm.
5. Glycogenesis.
6. They close, because the extra ATP from respiration shuts them.
7. 78 ÷ 12 = 6.5 units.
8. (12.4 − 7.0) ÷ 1.5 = 3.6 mmol dm⁻³ per hour.
9. (5.2 − 9.6) ÷ 9.6 × 100 = −46%, a fall of 46%.
10. Bacteria cannot remove introns from RNA.

Must-know distinctions

Pair	Difference
Endocrine and exocrine	Endocrine secretes into blood with no duct. Exocrine secretes along a duct
Cortex and medulla	Cortex makes steroid hormones over hours and days. Medulla makes adrenaline within seconds of nerve stimulation
Alpha and beta cells	Alpha cells release glucagon when glucose is low. Beta cells release insulin when glucose is high
Insulin and glucagon	Insulin lowers blood glucose. Glucagon raises it
Glucagon and adrenaline	Both raise blood glucose through cAMP, but glucagon is released in response to low glucose, adrenaline in response to stress
Type 1 and Type 2	Type 1 is a shortage of insulin. Type 2 begins as a poor response to insulin
Insulin injections and stem cells	Injections replace the hormone. Stem cells aim to replace the cells that make it

Reading a graph or table

1. Quote values with units from the axes.
2. Calculate a percentage change or a rate when the question gives numbers.
3. Link the pattern to the mechanism, for example a rise in insulin after a glucose peak shows beta cells responding.
4. Say what the data cannot show, such as the cause of a difference between two people.

Worked reminder. Glucose is 8.2 mmol dm⁻³ at 0 minutes and 12.0 at 60 minutes. Percentage rise = (12.0 − 8.2) ÷ 8.2 × 100 = 46%. If it has not returned to 8.2 by 180 minutes, the feedback is not restoring the starting level, which fits diabetes.

Where marks are usually lost

• Writing that the pancreas stores glycogen or converts glucose. The liver and muscle do this.
• Saying insulin “enters” cells instead of binding to a surface receptor.
• Mixing up glycogenesis, glycogenolysis and gluconeogenesis.
• Leaving out a step in the beta cell sequence, or reversing the order of depolarisation and calcium entry.
• Describing negative feedback without saying that the response reverses the change.
• Omitting units or the conversion between millimetres and micrometres in magnification answers.
• Calling Type 2 diabetes a simple lack of insulin.
• Giving only advantages of stem cell treatment, with no mention of rejection, ethics or limited evidence.

Official syllabus

OCR Level 3 Advanced GCE in Biology A (H420), Version 4.1 (April 2026), for first assessment in 2025, published by OCR. These notes cover 5.1.4(a) to 5.1.4(f).