OxfordAQA International AS and A-level Biology: Blood glucose and diabetes (9610) – Revision Notes

These notes condense section 3.4.7 of the OxfordAQA International AS and A-level Biology (9610) specification, Version 5.1: 3.4.7.1 to 3.4.7.4. For full explanations and worked examples, use the study guide. When the notes feel secure, try the practice questions. The course hub is OxfordAQA A-level Biology, the printable list is the checklist, and the free diagnostics show which topics need most work.

3.4.7.1 Glucose concentration and its control

Why stability matters

If glucose is	Effect	Reason
Too low	Weakness, confusion, loss of consciousness	Less respiration, so less ATP for cells, particularly brain cells
Too high	Cells lose water	The blood’s water potential drops, so water moves out of cells osmotically

Factors that change blood glucose: carbohydrate in the diet and its digestion and absorption; use of glucose in respiration (more during exercise); the liver’s release or storage of glucose; the hormones insulin, glucagon and adrenaline.

Liver processes

Term	Meaning	Trigger
Glycogenesis	glucose to glycogen	high blood glucose
Glycogenolysis	glycogen to glucose	low blood glucose, stress
Gluconeogenesis	glycerol and amino acids to glucose	low blood glucose, glycogen depleted

Memory trick. Genesis is creation (of glycogen), lysis is splitting (of glycogen), and neo means new (new glucose from non-carbohydrate).

Diabetes at a glance

	Type 1	Type 2
Cause	immune system destroys the insulin-making cells; little or no insulin	target cells respond poorly to insulin; insulin may also fall
Risk factors	genetic predisposition, family history	obesity, inactivity, poor diet, age, family history
Control	insulin injections plus diet and monitoring	diet, weight loss and exercise first; insulin if needed

Why injected? Insulin is a protein and would be digested by proteases if swallowed.

Explaining symptoms: the chain to write

1. Glucose too high, so the kidney tubule cannot reabsorb it all (carrier proteins saturated), and it appears in urine.
2. Dissolved glucose holds water in the tubule, so less is recovered and urine volume rises.
3. Water loss makes the blood’s water potential fall, so the person is thirsty.
4. Cells cannot take up glucose, so they respire fats and proteins, causing tiredness and weight loss.

Method for risk-factor data

1. Quote figures from the table or graph, with units.
2. Calculate a ratio or percentage change to compare groups.
3. State the trend: positive or negative correlation.
4. Say correlation is not proof of cause; name possible confounding variables.
5. Comment on sample size and how the groups were chosen.
6. Link to a mechanism if you can.

Worked reminder. Incidence is 2.2 cases per 1000 per year in the lowest-risk group and 16.5 in the highest. Ratio = 16.5 ÷ 2.2 = 7.5, so the highest group is 7.5 times as likely to develop the disease.

3.4.7.2 Insulin

Protein hormone, from the pancreas, carried in blood. It acts only on cells with matching receptors.

1. Attaches to receptors on the surface of target cells.
2. Controls glucose uptake by regulating the inclusion of channel proteins in the surface membrane.
3. Activates enzymes that convert glucose to glycogen.

Result: blood glucose falls.

3.4.7.3 Glucagon

Protein hormone, from the pancreas, acting on target cells.

1. Attaches to receptors on the surface of target cells.
2. Activates enzymes converting glycogen to glucose.
3. Activates enzymes making glucose from glycerol and amino acids.

Result: blood glucose rises.

3.4.7.4 Adrenaline and the second messenger model

Adrenaline attaches to receptors on the surface of target cells and activates enzymes converting glycogen to glucose.

Second messenger sequence (write in this order)

1. Hormone (first messenger) binds to its receptor on the cell surface.
2. Adenyl cyclase inside the membrane is activated.
3. Adenyl cyclase turns ATP into cAMP, the second messenger.
4. Protein kinase is switched on by cAMP.
5. Protein kinase then activates the enzymes that break glycogen down to glucose.

Why it is useful: the hormone does not enter the cell, and one hormone molecule produces many cAMP molecules, so the response is amplified.

Two model chains to learn

After a carbohydrate-rich meal

1. Glucose is absorbed and blood glucose rises above the set point.
2. Pancreatic cells secrete more insulin, which travels in the blood.
3. Insulin binds to receptors on the surface of liver, muscle and fat cells.
4. More channel proteins are inserted into the membranes, so uptake of glucose increases.
5. Enzymes that convert glucose to glycogen are activated.
6. Blood glucose falls back towards the set point, and insulin secretion falls.

Between meals or during exercise

1. Blood glucose falls below the set point.
2. Glucagon is released and attaches to receptors on liver cells; in stress or exercise adrenaline does the same.
3. Both use cAMP as a second messenger and activate enzymes that convert glycogen to glucose.
4. Glucagon also switches on enzymes that make glucose from glycerol and amino acids.
5. Glucose enters the blood and the concentration rises.

Because each chain reverses the other’s effect, the system shows negative feedback.

Data skills

Skill	Formula or step	Example
Percentage change	(new − old) ÷ old × 100	6.0 to 9.0 is a rise of 50%
Mean rate	change ÷ time	3.0 mmol dm⁻³ in 30 min is 0.10 mmol dm⁻³ min⁻¹
Fold change	treated ÷ control	12 ÷ 3 is a 4-fold rise
Risk ratio	incidence in one group ÷ incidence in baseline group	8.4 ÷ 2.1 is 4

Reading a glucose tolerance curve

• Start value: is it within the typical fasting range of about 4 to 6 mmol dm⁻³?
• Peak: how high, and how long after the drink?
• Return: how quickly does it fall back to the start value? A slow or incomplete fall suggests poor regulation.

Reading a hormone experiment

• Compare each treatment with the control, not with other treatments.
• If blocking one step removes the effect of the hormone, that step is needed.
• If adding a later component gives the effect without the hormone, that component acts after the receptor.
• Use figures from the table in your answer.

Command words

• Explain: give the reason, not only the event.
• Describe: state what happens in order.
• Suggest: apply what you know to a new situation.
• Evaluate: weigh strengths and limitations, then reach a judgement.

Must-know distinctions

Pair	Difference
Glycogen and glucagon	glycogen is the storage polysaccharide; glucagon is the hormone
Insulin and glucagon	opposite effects: glucose to glycogen, and glycogen to glucose
Glucagon and adrenaline	both use the second messenger model; both raise blood glucose; adrenaline is released in stress or exercise
Type 1 and Type 2	Type 1 is a lack of insulin; Type 2 is poor response to insulin
Glycogenolysis and gluconeogenesis	the substrate: glycogen versus glycerol and amino acids

Quick self-test

1. Explain why a very high blood glucose concentration harms cells.
2. Name the process that makes glucose from amino acids.
3. A reading falls from 9.8 to 6.2 mmol dm⁻³. Calculate the percentage fall.
4. Glucose falls from 11.4 to 7.2 mmol dm⁻³ in 90 minutes. Calculate the mean rate of fall in mmol dm⁻³ per hour.
5. Which enzyme makes cAMP, and from what?
6. Why is insulin not taken as a tablet?
7. Give two ways insulin makes target cells take up and store glucose.
8. Why does insulin affect only some cells?
9. Name the first and second messengers in the adrenaline pathway.
10. Why is glycogen a better store than free glucose?
11. State two risk factors for Type 2 diabetes.
12. Why does a person with untreated diabetes produce a large volume of urine?

Answers

1. Dissolved glucose lowers the blood’s water potential, and water moves out of cells by osmosis.
2. Gluconeogenesis.
3. (9.8 − 6.2) ÷ 9.8 × 100 = 37% (36.7%).
4. (11.4 − 7.2) ÷ 1.5 = 2.8 mmol dm⁻³ per hour.
5. Adenyl cyclase, from ATP.
6. It is a protein, so proteases in the gut would digest it.
7. It inserts more channel proteins into the membrane, and it activates enzymes that convert glucose to glycogen.
8. Only target cells have receptors complementary to insulin.
9. First: adrenaline. Second: cAMP.
10. Glycogen is large and insoluble, so it has almost no effect on water potential, and it can be rapidly broken down when needed.
11. Any two of: obesity, inactivity, a diet high in refined sugar and fat, increasing age, family history.
12. Glucose stays dissolved in the filtrate and holds water in the tubule, so less water is recovered.

Where marks are usually lost

• Writing “insulin converts glucose to glycogen” rather than “activates enzymes”.
• Leaving out water potential when explaining the danger of high glucose.
• Describing receptors as taking in glucose. The hormone binds the receptor; glucose crosses by channel proteins.
• Confusing glycogen and glucagon, or glycogenesis and glycogenolysis.
• Omitting adenyl cyclase, cAMP or protein kinase, or giving them out of order.
• Saying the hormone “enters” the cell in the second messenger model.
• Giving the same cause for Type 1 and Type 2.
• Stating that a correlation in risk-factor data proves cause.
• Quoting a percentage change without the units or the starting value as the denominator.

Official syllabus

OxfordAQA, International AS and A-level Biology (9610), Version 5.1, for International A-level exams May/June 2018 onwards: section 3.4.7, Hormones and the control of blood glucose concentration.