OxfordAQA International AS and A-level Biology: Blood glucose control, hormones and diabetes (9610)

This guide follows the OxfordAQA International AS and A-level Biology (9610) specification, Version 5.1. It covers section 3.4.7, Hormones and the control of blood glucose concentration: 3.4.7.1 (glucose concentration and its control), 3.4.7.2 (insulin), 3.4.7.3 (glucagon) and 3.4.7.4 (adrenaline and the second messenger model). In the specification, Unit 4 (Control) is one of the units that belong to the International A-level only.

Afterwards, condense with the revision notes and check yourself on the practice questions. The course hub is OxfordAQA A-level Biology, the printable list is the checklist, and the free diagnostics point to weak spots.

Scope of section 3.4.7

Section	Outcomes
3.4.7.1	Explain why blood glucose must be stable (energy transfer, water potential); name the factors that change it; describe glycogenesis, glycogenolysis and gluconeogenesis in the liver; give the causes and risk factors of the two main types of diabetes, and how diet and insulin control each; explain symptoms; analyse, interpret and evaluate risk-factor data
3.4.7.2	Describe insulin as a protein hormone acting through surface receptors, channel proteins and enzymes
3.4.7.3	Describe glucagon acting through receptors and enzymes that release glucose
3.4.7.4	Describe adrenaline’s action and the second messenger model with adenyl cyclase, cAMP and protein kinase

3.4.7.1 Why blood glucose must stay stable

Glucose is the main respiratory substrate. Every cell needs a steady supply to make ATP, and some tissues, the brain especially, depend heavily on it. The two risks mirror each other.

• Too low (hypoglycaemia). Respiration slows, so less ATP is made and active processes such as nerve conduction falter. You may feel confused, shaky or faint.
• Too high (hyperglycaemia). Dissolved glucose lowers the water potential of the blood plasma. Water then leaves cells by osmosis down the water potential gradient, so cells lose water and may become dehydrated.

A typical fasting concentration is about 4 to 6 mmol dm⁻³. Do not write “constant”: the value varies a little around a set point, which is why the word stable is safer.

Factors that change blood glucose

Raises it	Lowers it
Absorption of glucose after digesting carbohydrate	Uptake into cells for respiration, which rises during exercise
Glycogenolysis in the liver	Glycogenesis in the liver
Gluconeogenesis in the liver	Uptake into muscle and fat cells under insulin

Hormone levels sit behind this table. Insulin lowers glucose; glucagon and adrenaline raise it.

The liver’s three processes

Process	Change	Occurs when
Glycogenesis	glucose to glycogen	blood glucose is high
Glycogenolysis	glycogen to glucose	blood glucose is low or in stress
Gluconeogenesis	glycerol and amino acids to glucose	stores of glycogen are running low

Glycogen is a branched polymer of glucose stored in liver and muscle cells. Because it is insoluble and large, it has almost no effect on water potential, unlike the same number of free glucose molecules. Note that gluconeogenesis makes glucose from non-carbohydrate molecules.

Diabetes

Diabetes is a failure of blood glucose control. After a meal the concentration stays too high, and the body cannot return it to normal.

	Type 1	Type 2
Cause	The immune system destroys the insulin-secreting cells of the pancreas, so little or no insulin is made. A genetic predisposition is a risk factor.	Target cells respond poorly to insulin (fewer or less responsive receptors), and insulin production may also fall.
Risk factors	Family history; usually appears in childhood or early adult life	Obesity, low physical activity, a diet rich in refined sugar and fat, increasing age, family history
Control	Injections of insulin matched to diet and activity; regular monitoring	Regulating carbohydrate intake, losing weight, increasing exercise; insulin only if these fail

Insulin is a protein, so it is injected rather than swallowed. A tablet would be digested by proteases in the gut and the hormone destroyed. Controlling the timing and amount of carbohydrate (especially refined sugars) helps both types, because it limits the peaks in blood glucose.

Explaining symptoms

Use the biology, not just the label. For untreated high glucose:

1. Glucose in the urine. The kidney tubules cannot reabsorb all the filtered glucose, because carrier proteins become saturated.
2. Large volumes of urine. Dissolved glucose keeps water in the tubule, so the kidney recovers less water and the urine volume rises.
3. Thirst. The body loses water and the blood’s water potential falls, so more fluid is drunk.
4. Tiredness and weight loss. Cells cannot take up glucose, so they respire less, and fats and proteins are broken down for energy instead.

Worked example: a glucose tolerance test

Two adults fasted, then drank a glucose solution at time 0. Blood glucose (mmol dm⁻³):

Time / min	0	30	60	90	120	180
Person X	4.7	8.9	7.1	5.6	4.9	4.6
Person Y	8.1	15.7	17.3	16.4	14.8	12.9

1. Percentage rise for X in the first 30 minutes = (8.9 − 4.7) ÷ 4.7 × 100 = 89%.
2. Mean rate of fall for X from 30 to 120 minutes = (8.9 − 4.9) ÷ 90 = 0.044 mmol dm⁻³ min⁻¹.
3. Mean rate of fall for Y from 60 to 180 minutes = (17.3 − 12.9) ÷ 120 = 0.037 mmol dm⁻³ min⁻¹.
4. Interpretation: X’s glucose returns to its starting range within about two hours, so regulation works. Y starts above the typical fasting range, peaks later and higher, and at 180 minutes is still 4.8 mmol dm⁻³ above its own fasting value (12.9 − 8.1), so Y’s glucose is not being removed effectively. This pattern fits diabetes, though one test cannot say which type.

Evaluating risk-factor data

Incidence is the number of new cases in a group over a period.

Body mass index	Under 25	25 to 29.9	30 to 34.9	35 or over
New Type 2 cases per 1000 people per year	1.8	4.5	11.7	22.1

Dividing each by 1.8 gives risks of 1.0, 2.5, 6.5 and 12.3 times the lowest group. Incidence rises steadily with body mass index, so there is a positive correlation. A correlation alone does not prove cause. To evaluate, ask whether the groups were similar in age, diet and activity (these are confounding variables), how many people were followed, and whether a plausible mechanism exists. Here one does: excess fat is linked with cells responding less to insulin.

3.4.7.2 The role of insulin

Insulin is a protein hormone made by the pancreas. It travels in the blood but acts only on target cells, those with matching receptors, such as liver, muscle and fat cells. It acts in three ways.

1. It attaches to receptors on the surface of target cells. The receptor’s shape is complementary to insulin, so other cells ignore it.
2. It increases glucose uptake by controlling the inclusion of channel proteins in the surface membrane. More channels in the membrane means faster facilitated diffusion of glucose into the cell.
3. It activates enzymes that convert glucose to glycogen, which keeps the concentration gradient into the cell steep.

The net result is that blood glucose falls.

3.4.7.3 The role of glucagon

Glucagon is also a protein hormone from the pancreas. It acts mainly on liver cells when blood glucose is low.

1. It attaches to receptors on the surface of target cells.
2. It activates enzymes that convert glycogen to glucose (glycogenolysis).
3. It switches on enzymes that make glucose from glycerol and amino acids (gluconeogenesis).

Glucose then leaves the liver into the blood and the concentration rises. Insulin and glucagon have opposite effects, which is the basis of negative feedback in this system.

3.4.7.4 The role of adrenaline and the second messenger model

Adrenaline is released in stress and during exercise. It also attaches to receptors on the surface of target cells and activates enzymes that convert glycogen to glucose, supplying glucose for respiration.

Adrenaline and glucagon cannot enter the cell, so a second messenger relays the signal. The hormone is the first messenger.

1. The hormone binds to its receptor on the outer surface of the membrane.
2. This activates the enzyme adenyl cyclase on the inside of the membrane.
3. Adenyl cyclase turns ATP into cyclic AMP (cAMP). This is the second messenger.
4. Protein kinase is switched on by cAMP.
5. Protein kinase in turn activates the enzymes that break glycogen down to glucose.

The cascade amplifies the signal: one bound hormone molecule leads to many cAMP molecules, and each activated enzyme works on many substrate molecules, so a tiny amount of hormone has a large effect.

Worked example: interpreting an experiment

Cultured liver cells were treated for 20 minutes. The rise in glucose in the surrounding solution was measured (arbitrary units):

Treatment	Glucose released
No hormone	2
Adrenaline	18
Adrenaline plus a drug that blocks adrenaline receptors	3
A drug that activates adenyl cyclase directly (no adrenaline)	17

1. Adrenaline raised the rise in glucose 18 ÷ 2 = 9-fold.
2. The receptor blocker cut it to 3, close to the control, so adrenaline needs its receptor to have any effect.
3. Activating adenyl cyclase directly gave 17, almost the adrenaline value, so adenyl cyclase acts after the receptor and no hormone is needed once it is switched on.

Common errors

• Writing that insulin “converts glucose to glycogen”. Insulin activates enzymes that do it.
• Saying glucose “enters through the receptor”. The receptor binds the hormone; glucose uses separate channel proteins.
• Mixing up glycogen (the store) and glucagon (the hormone).
• Giving only “hormone binds to receptor” for the second messenger model. Name adenyl cyclase, cAMP and protein kinase in order.
• Describing hyperglycaemia without water potential, or missing that Type 1 and Type 2 have different causes.

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.