Blood glucose concentration must be maintained within narrow limits, because levels that are too high or too low can damage cells or prevent them functioning effectively (as explored below).
Why does blood glucose need to be controlled?
Why does blood glucose need to be controlled?
- Too high — lowers the water potential of the blood. This can cause water to move out of cells by osmosis, potentially damaging them.
- Too low — cells don’t have enough glucose for respiration, so they can’t produce sufficient ATP for energy-requiring processes.
This is an example of homeostasis regulated by hormones secreted from the islets of Langerhans in the pancreas.
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The factors that influence blood glucose concentration.
The role of the liver in glycogenesis, glycogenolysis and gluconeogenesis.
The Pancreas & Islets of Langerhans
The islets of Langerhans are clusters of hormone-secreting cells scattered throughout the pancreas:
| Cell type | Hormone secreted | Response to… |
|---|---|---|
| Alpha (α) cells | Glucagon | Low blood glucose |
| Beta (β) cells | Insulin | High blood glucose |
Tip
Don’t confuse the islets of Langerhans (endocrine: secrete hormones into blood) with the acinar cells of the pancreas (exocrine: secrete digestive enzymes into the gut).
Genesis & Lysis
Key phrases you need to understand:
-
Glycogenolysis
- Breakdown of glycogen to glucose (when blood glucose levels are too low)
- Liver & muscle cells
-
Glycogenesis
- Synthesis of glycogen from glucose (when blood glucose levels are too high)
- Removes glucose from the bloodstream by converting it to glycogen (a storage molecule)
- Liver & muscle cells
-
Gluconeogenesis
- Synthesis of glucose from non-carbohydrate molecules (e.g. amino acids, glycerol)
- Liver cells
Tip
Think about the word: genesis = creation, lysis = splitting/breaking down. So glycogenesis = creation of glycogen. Glycogenolysis = breaking down of glycogen.
High Blood Glucose → Insulin (Beta Cells)
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The action of insulin by:
- attaching to receptors on the surfaces of target cells
- controlling the uptake of glucose by regulating the inclusion of channel proteins in the surface membranes of target cells
- activating enzymes involved in the conversion of glucose to glycogen.
When blood glucose rises (e.g. after a meal):
-
Beta cells detect the rise and secrete insulin into the blood
-
Insulin binds to specific receptors on the cell surface membrane of target cells e.g. liver, muscle, and adipose cells. Insulin has a complementary shape to the insulin receptor. A change in the amino acid sequence of insulin (e.g. neonatal diabetes) can change its tertiary structure, so it is no longer complementary to the insulin receptor.
-
Insulin triggers movement and fusion of vesicles containing glucose transporter proteins (GLUT4) with the cell membrane, increasing the number of glucose transporter (GLUT4) carrier proteins, so more glucose enters the cell by facilitated diffusion, removing glucose from the bloodstream
-
Insulin also activates enzymes for glycogenesis which convert glucose → glycogen
As a result of the above changes, this causes:
- Increased rate of absorption of glucose into cells (muscle cells especially)
- Increased rate of cellular respiration: more glucose is available inside the cells (via GLUT4), so more substrate is available for respiration
- Increased conversion of glucose to glycogen
Low Blood Glucose → Glucagon (Alpha Cells)
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The action of glucagon by:
- attaching to receptors on the surfaces of target cells
- activating enzymes involved in the conversion of glycogen to glucose
- activating enzymes involved in the conversion of glycerol and amino acids into glucose.
When blood glucose falls (e.g. between meals, during exercise):
-
Alpha cells detect the fall and secrete glucagon into the blood
-
Glucagon binds to receptors on target cells (main target is liver cells)
-
Acts via the second messenger model (see below)
-
Activates glycogenolysis — enzymes break down glycogen → glucose, released into blood
-
Activates gluconeogenesis — glucose synthesised from non-carbohydrate precursors:
- Glycerol
- Amino acids (from protein breakdown)
Tip
Glycerol, not fatty acids, is used in gluconeogenesis
Adrenaline (Fight or Flight)
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The role of adrenaline by:
- attaching to receptors on the surfaces of target cells
- activating enzymes involved in the conversion of glycogen to glucose.
Adrenaline is released from the adrenal medulla (adrenal glands) in response to stress or exercise, triggered by the nervous system, not blood glucose levels directly.
- Binds receptors on liver and muscle cells
- Activates glycogenolysis (glycogen → glucose)
- Inhibits glycogenesis
- Promotes glucagon secretion, inhibits insulin secretion
- Acts via the second messenger model (same cAMP pathway as glucagon)
Tip
Unlike insulin and glucagon, adrenaline responds to stress/fear/exercise via the nervous system, not directly to blood glucose concentration. It raises blood glucose as part of preparing the body for rapid action, regardless of current glucose levels.
Second Messenger Model (cAMP)
Glucagon and adrenaline both work via the second messenger model:
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The second messenger model of adrenaline and glucagon action, involving adenylate cyclase, cyclic AMP (cAMP) and protein kinase.
- Hormone (glucagon/adrenaline) = first messenger — binds complementary receptor on cell surface membrane
- This causes the receptor to change shape inside the cell membrane. This activates the enzyme adenylate cyclase
- Adenylate cyclase converts ATP → cAMP (second messenger)
- cAMP activates protein kinase A
- Protein kinase A activates conversion of glycogen to glucose (glycogenolysis) and inhibits glycogenesis
Tip
The hormone is the first messenger, cAMP is the second messenger. The receptor is not the first messenger.
Diabetes
What you need to know (from the AQA specification)
What you need to know (from the AQA specification)
The causes of types I and II diabetes and their control by insulin and/or manipulation of the diet.
Students should be able to evaluate the positions of health advisers and the food industry in relation to the increased incidence of type II diabetes.
| Type 1 | Type 2 | |
|---|---|---|
| Cause | Autoimmune destruction of β cells | Insulin resistance (cells less responsive) |
| Insulin production | None | Reduced or normal but ineffective |
| Onset | Usually childhood/young adult | Usually adult onset |
| Treatment | Insulin injections | Diet, exercise, medication |
What does reduced insulin sensitivity mean?
What does reduced insulin sensitivity mean?
Target cells have fewer insulin receptors or the receptors are less responsive to insulin. This means even when insulin is present, cells don’t take up glucose as effectively, so blood glucose remains high.
How this topic is tested
This analysis is based on past paper data from 2017 to 2025. It is intended for interest only and is not predictive of what will appear in future papers.
- Tested in 8 of 9 years (2017–2025): 19 question parts worth 44 marks.
- 24th most-examined topic overall by marks, 5th in Unit 6.
Marks by year
Most-tested spec points
- Types I and II Diabetes: tested in 10 parts (26 marks)
- The Action of Insulin: tested in 4 parts (8 marks)
- The Second Messenger Model: tested in 2 parts (4 marks)
- The Action of Glucagon: tested in 2 parts (3 marks)
- Blood Glucose & the Role of the Liver: tested in 1 part (2 marks)
Also links to: Facilitated Diffusion, Other Respiratory Substrates, DNA Structure.
Maths and practical skills
- Units and standard form (MS 0.1, 0.2): e.g. 2022 P2 Q8.1
- Percentages, ratios and fractions (MS 0.3): e.g. 2024 P2 Q9.3
- Significant figures (MS 1.1): e.g. 2019 P2 Q5.2
Tips from examiner reports
What students commonly get wrong
- Glucagon activates enzymes; it isn't an enzymeWatch out: glucagon is a hormone, so it doesn't convert anything itself. It binds to receptors on liver cells and activates enzymes that convert glycerol and amino acids into glucose. 2019 P2 Q5.1
- Glycogenesis, glycogenolysis, gluconeogenesisWatch out: the names tell you what happens. Glycogenesis makes glycogen from glucose; glycogenolysis breaks glycogen down to glucose; gluconeogenesis makes new glucose from glycerol and amino acids. Glycolysis is the first stage of respiration, and glucagon is the hormone. 2019 P2 Q5.3 · 2019 P2 Q5.4 · 2024 P2 Q2.3
- How insulin increases glucose uptakeWatch out: insulin doesn't open existing channels. It causes vesicles containing channel (carrier) proteins to fuse with the cell-surface membrane, so there are more of these proteins and more glucose enters by facilitated diffusion. The vesicles contain the channel proteins, not glucose. 2018 P3 Q1.3 · 2021 P2 Q5.2
- cAMP is made from ATPWatch out: adenylate cyclase converts ATP into cAMP. cAMP then activates protein kinase, which activates the enzymes that convert glycogen to glucose. 2019 P2 Q5.4
- Insulin is complementary to its receptorWatch out: insulin is a hormone, not an enzyme or substrate. A change in its tertiary structure means it's no longer complementary to its receptor, so it can't bind. 2021 P2 Q5.1
- Type II: the cells are less sensitive to insulinWatch out: in type II diabetes, insulin is still made, but the cells' receptors are less sensitive (responsive) to it. Link it to specific risk factors (weight, diet, lack of exercise) rather than "lifestyle". 2024 P2 Q9.1
Exam Question Practice
Type II diabetes is in remission when a person’s blood glucose concentration stays below the level used to diagnose diabetes for at least 3 months, without any diabetes medication.
Scientists investigated whether a low-calorie diet programme could put type II diabetes into remission.
Give two reasons why a diet programme could be used to treat type II diabetes but not type I diabetes.
(2 marks)
Hint
Compare the two types. Is insulin made? How do the target cells respond to it? What is each type linked to?
Mark Scheme
Max 2 marks
- People with type I diabetes do not produce insulin, or people with type II diabetes still produce insulin (1 mark)
- In type II diabetes, the receptors (cells) are less responsive to insulin (1 mark)
- Type II diabetes is linked to body mass (obesity), but type I is not (1 mark)
Also accepted / rejected
Tips
- Type I means no insulin is made. In type II, insulin is still made
- Say the receptors or cells are less responsive to insulin, not “the body”
- Link type II to body mass, diet or exercise, not just “lifestyle”
Also accepted