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

This guide covers topic 5.1.4, Hormonal communication, in Module 5 of the OCR A Level Biology A (H420) specification, Version 4.1 (April 2026), for first assessment in 2025. The specification uses Type 1 diabetes as its example of medical technology regulating a hormonal system. Condensed recall is in the revision notes and exam-style questions are in the practice set. Find your next topic on the OCR A Level Biology hub, tick it off on the checklist, and use the free diagnostics to spot weak areas.

Outcomes in this topic

Outcome	What you must be able to do
5.1.4(a)	Explain endocrine communication: secretion into the blood, transport by the blood, detection by target cells or tissues
5.1.4(b)	Describe the structure and functions of the adrenal glands, including the hormones of the cortex and medulla
5.1.4(c)	Describe the histology of the pancreas, including the endocrine tissues; examine and draw stained sections (PAG1, HSW4)
5.1.4(d)	Explain how blood glucose is regulated: insulin and glucagon as negative feedback, the role of the liver, and control of insulin secretion through potassium and calcium channels in beta cells
5.1.4(e)	Explain the differences between Type 1 and Type 2 diabetes mellitus, with causes and treatments
5.1.4(f)	Evaluate treatments: insulin from genetically modified bacteria, and the potential use of stem cells

5.1.4(a) Endocrine communication

A hormone is a chemical messenger made by an endocrine gland, a gland with no duct. Hormones pass straight into the blood. Communication has three stages:

1. Secretion. The gland cells release the hormone into the blood capillaries around them, usually by exocytosis.
2. Transport. The blood carries the hormone to every part of the body. Every tissue is reached, but only some respond.
3. Detection. Target cells carry receptors with a shape complementary to the hormone. Other cells ignore it.

Water-soluble hormones (insulin, glucagon, adrenaline) cannot cross the phospholipid bilayer. Their receptor is in the cell surface membrane, and it triggers an internal signalling pathway, often with a second messenger. Steroid hormones (cortisol, aldosterone) are lipid-soluble, so they cross the membrane and bind receptors inside the cell. The complex alters gene transcription, so the response is slower.

Compared with the nervous system, endocrine communication is slower, lasts longer and acts widely.

5.1.4(b) The adrenal glands

There are two adrenal glands, one above each kidney. Each has an outer cortex and an inner medulla.

Region	Hormones	Main functions
Cortex	Mineralocorticoids, mainly aldosterone	Raise sodium ion reabsorption and potassium ion loss in the kidney tubules, which helps maintain blood volume and blood pressure
Cortex	Glucocorticoids, mainly cortisol	Raise blood glucose (including by gluconeogenesis), reduce inflammation, help with long-term stress
Medulla	Adrenaline and noradrenaline	Short-term “fight or flight” preparation

The medulla is stimulated directly by sympathetic neurones, so it links the nervous and endocrine systems.

Adrenaline raises heart rate, widens the bronchioles, diverts blood to muscles and away from the gut, and triggers glycogenolysis, so more glucose is available for respiration. It raises blood glucose, so it opposes insulin.

5.1.4(c) Histology of the pancreas

The pancreas is a mixed gland with two tissues.

• Exocrine tissue makes up most of the organ. Clusters of cells called acini (singular acinus) make digestive enzymes, which leave through ducts into the small intestine. Acinar cells contain zymogen granules and stain darkly.
• Endocrine tissue forms the islets of Langerhans: small, pale-staining patches scattered through the acini. Islets have no ducts. They have a rich capillary network, so hormones enter the blood quickly.

Two cell types in the islets matter for this topic.

Cell type	Hormone made	Triggered by
Alpha cells	Glucagon	Low blood glucose
Beta cells	Insulin	High blood glucose

With a routine stain you can find the islets, but you cannot tell alpha from beta cells. That needs special stains or antibody labelling.

Examining and drawing a section (PAG1, HSW4)

1. On low power, find a pale islet among the darker acini.
2. Make a tissue plan: outlines only, with no individual cells.
3. Switch to high power and make a cell drawing of a small area, showing a few cells and nuclei.
4. Draw large, in pencil, with unbroken lines and no shading.
5. Add ruled label lines that do not cross.
6. Add a title, then record the magnification and a scale bar.

Worked example: magnification from a scale bar. Your drawing of an islet is 48 mm across. The scale bar beside it is 20 mm long and is labelled 100 micrometres (µm).

1. Actual width = 48 ÷ 20 × 100 = 240 µm.
2. Magnification = drawn length ÷ actual length = 20 mm ÷ 0.100 mm = ×200.

Convert units first: 1 mm is 1000 µm.

5.1.4(d) Regulating blood glucose

Too little glucose starves cells. Too much lowers the water potential of the blood. In a healthy fasting person the concentration is roughly 4 to 6 mmol dm⁻³.

Negative feedback with insulin and glucagon

Beta and alpha cells detect blood glucose directly. The liver and muscle are the main effectors.

	Blood glucose too high	Blood glucose too low
Detected by	Beta cells	Alpha cells
Hormone	Insulin released	Glucagon released
Response	More glucose enters cells; liver and muscle convert glucose to glycogen; more glucose is respired	Liver converts glycogen to glucose and makes glucose from non-carbohydrates
Result	Blood glucose falls	Blood glucose rises

This is negative feedback: the response reverses the original change, and as the level returns to normal the stimulus weakens, so less hormone is released. Two opposing hormones give finer control.

The role of the liver

The liver receives blood from the gut through the hepatic portal vein, so it sees absorbed glucose first. Its cells (hepatocytes) carry out three processes:

• Glycogenesis: glucose to glycogen, lowering blood glucose.
• Glycogenolysis: glycogen to glucose, raising blood glucose.
• Gluconeogenesis: glucose made from non-carbohydrate sources such as amino acids and glycerol, raising blood glucose.

Insulin promotes glycogenesis. Glucagon promotes glycogenolysis and gluconeogenesis. In muscle and fat, insulin also increases the number of glucose transporters in the surface membrane.

Glucagon binds to a receptor on the hepatocyte surface, which activates adenylyl cyclase. This makes cyclic AMP (cAMP) from ATP, and cAMP acts as a second messenger that starts an enzyme cascade. Adrenaline uses the same type of pathway. The signal is amplified at each step.

Control of insulin secretion in beta cells

Beta cells secrete insulin only when glucose is high. The mechanism links glucose metabolism to the membrane.

1. Glucose enters the beta cell by facilitated diffusion through a glucose transporter. More glucose outside means more glucose inside.
2. The cell respires it, so the ATP concentration rises.
3. ATP closes potassium ion channels in the surface membrane. Potassium ions can no longer leave.
4. The inside of the cell becomes less negative: the membrane depolarises.
5. Depolarisation opens voltage-gated calcium ion channels. Calcium ions diffuse in.
6. The rise in calcium ion concentration makes vesicles containing insulin fuse with the surface membrane. Insulin is released by exocytosis.

At low glucose, little ATP is made, the potassium channels stay open, the membrane stays polarised, the calcium channels stay shut and little insulin is released.

Worked example: islet data. Isolated islets were kept in solutions of different glucose concentration, and insulin released was measured as picomoles per islet per hour.

Glucose / mmol dm⁻³	2	5	8	11	14
Insulin released	0.4	0.5	1.8	4.6	5.0

At 5 mmol dm⁻³, adding a drug that closes potassium channels gave 4.2. At 11 mmol dm⁻³, adding a calcium channel blocker gave 0.6.

(i) Percentage increase from 5 to 11 mmol dm⁻³: (4.6 − 0.5) ÷ 0.5 × 100 = 820%.

(ii) Mean change from 8 to 11 mmol dm⁻³: (4.6 − 1.8) ÷ 3 = 0.93 pmol islet⁻¹ h⁻¹ per mmol dm⁻³.

(iii) The potassium channel blocker raised release 4.2 ÷ 0.5 = 8.4 times at low glucose, so closing potassium channels is enough to cause release.

(iv) The calcium blocker cut release by (4.6 − 0.6) ÷ 4.6 × 100 = 87%, so calcium entry is needed.

5.1.4(e) Type 1 and Type 2 diabetes mellitus

In diabetes mellitus blood glucose stays too high (hyperglycaemia). Symptoms include thirst, frequent urination and weight loss. Glucose appears in the urine when it exceeds what the kidney tubules can reabsorb.

	Type 1	Type 2
Cause	Autoimmune destruction of beta cells, so little or no insulin is made. Genetic factors and an environmental trigger are thought to contribute	Target cells respond less to insulin (insulin resistance); beta cells may later fail to keep up
Risk factors	Family history	Obesity, inactivity, poor diet, age, family history and ethnic background
Insulin level	Very low	Normal or high at first
Main treatment	Insulin injections or a pump, blood glucose monitoring, carbohydrate management	Diet change, weight loss and exercise; drugs if needed; insulin later in some patients

Worked example: reading fasting data. Three adults were tested after fasting.

Person	Blood glucose / mmol dm⁻³	Insulin / pmol dm⁻³
P	4.9	58
Q	13.8	6
R	9.6	210

P has normal values. Q has high glucose and almost no insulin, which fits Type 1: the beta cells are not making it. R has high glucose and a high insulin level, 210 ÷ 58 = 3.6 times that of P. Insulin is present but not working properly, which fits Type 2 insulin resistance.

Treatments used

Type 2 drugs include metformin, which reduces glucose production by the liver and makes cells more responsive to insulin, and sulfonylureas, which close the potassium channels in beta cells and so stimulate insulin release (the same step as in the data above).

Type 1 is the specification’s example of medical technology regulating a hormonal system. A sensor measures glucose and insulin is delivered by injection or a pump. Some systems link the two so that the dose adjusts automatically, mimicking negative feedback.

5.1.4(f) Potential treatments

Insulin from genetically modified bacteria

Insulin once came from pigs and cattle. Human insulin is now made by genetically modified bacteria.

1. Obtain the human insulin gene without introns, because bacteria cannot remove them. It can be made from mRNA by reverse transcriptase or built from the known sequence.
2. Cut the gene and a plasmid with the same restriction enzyme, giving matching sticky ends, and join them with DNA ligase.
3. Insert the recombinant plasmid into bacteria. A marker gene, for example for antibiotic resistance, shows which took it up.
4. Grow the bacteria in a fermenter so that they express the gene.
5. Extract and purify the insulin, which must be in its active form.

Advantages: the insulin has the human amino acid sequence, so it is less likely to trigger an immune response; supply is large and reliable; and no animal tissue is needed, which avoids ethical and religious objections.

Stem cells

Stem cells can divide and differentiate. The idea is to grow them into beta cells or islet tissue and transplant these into a patient, so that the body regulates insulin itself. The evidence for this is still developing: trials in people have reported patients who no longer needed insulin injections, but the patients also needed immunosuppressant drugs, and it is not yet routine care.

• Benefit: a possible cure for Type 1 rather than lifelong management.
• Rejection: donor-derived cells are rejected unless the immune system is suppressed. Cells made from the patient’s own cells would avoid this.
• Autoimmunity: the immune attack that destroyed the original beta cells could target the new ones.
• Ethics and safety: embryonic stem cells raise objections, and uncontrolled division could cause tumours.

Common errors

• Writing that the pancreas “converts glucose to glycogen”. The liver and muscle do that, under the influence of insulin.
• Saying insulin enters cells. It binds to a surface receptor.
• Muddling the beta cell sequence: glucose, ATP, potassium channels close, depolarisation, calcium channels open, exocytosis.

Official syllabus

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