Control of blood glucose concentration (A-level only)
AQA
A-Level
Blood glucose concentration is influenced by diet, exercise, hormones and body mass. Glucose rises after a carbohydrate meal as gut enzymes hydrolyse starch and disaccharides and the products are absorbed from the small intestine. It falls when cells respire glucose, especially during exercise, and when the liver and muscle cells convert glucose to glycogen (glycogenesis) under the influence of insulin. During fasting, the liver breaks down glycogen to glucose (glycogenolysis) and can synthesise glucose from non-carbohydrate sources such as glycerol and amino acids (gluconeogenesis). Glucagon stimulates both glycogenolysis and gluconeogenesis, while adrenaline stimulates glycogenolysis. Body mass is a risk factor for type 2 diabetes rather than an acute control factor.
27
Objectives
26
Exam Tips
40
Pitfalls
48
Key Terms
49
Mark Points
Subtopics in this area
The factors that influence blood glucose concentration.
The role of the liver in glycogenesis, glycogenolysis and gluconeogenesis.
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.
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.
The role of adrenaline by: attaching to receptors on the surfaces of target cells activating enzymes involved in the conversion of glycogen to glucose.
The second messenger model of adrenaline and glucagon action, involving adenylate cyclase, cyclic AMP (cAMP) and protein kinase.
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.
Required practical 11: Production of a dilution series of a glucose solution and use of colorimetric techniques to produce a calibration curve with which to identify the concentration of glucose in an unknown ‘urine’ sample.
Control of blood glucose concentration (A-level only) Revision Guide
Learning Objectives
What you need to know and understand
- List factors that raise and lower blood glucose concentration.
- Explain how blood glucose concentration changes during exercise.
- Distinguish the roles of insulin, glucagon and adrenaline in blood glucose regulation.
- Define glycogenesis, glycogenolysis and gluconeogenesis and state the effect of each on blood glucose concentration.
- Explain what happens in the liver during prolonged fasting as glycogen stores fall.
- Explain why liver glycogen, but not muscle glycogen, can raise blood glucose concentration.
- Describe the ways insulin lowers blood glucose concentration after a meal.
- Explain why a cell whose receptors are faulty takes up glucose slowly even when the insulin concentration is high.
- Explain how the fall in blood glucose that insulin causes switches off its own secretion.
- Describe how glucagon raises blood glucose concentration, naming the cells that secrete it and its target cells.
- Explain why glucagon must act through a membrane receptor rather than entering liver cells.
- Compare the actions of insulin and glucagon on liver cells.
- Describe how adrenaline raises blood glucose concentration via cell-surface receptors.
- Explain the difference in glycogenolysis outcomes between liver and muscle cells.
- Understand the mechanism of enzyme activation involved in the conversion of glycogen to glucose.
- Sequence the second messenger model from hormone binding through to the release of glucose from glycogen.
- Explain why a hydrophilic hormone needs a second messenger rather than acting inside the cell directly.
- Explain how the cascade amplifies the effect of a very low hormone concentration.
- Explain the difference in cause between type I and type II diabetes in terms of insulin production and receptor sensitivity.
- Explain why insulin must be injected rather than taken by mouth.
- Evaluate data from a study as evidence that a high-fat diet is a risk factor for type II diabetes, commenting on species and duration.
- Construct an argument for and an argument against a food industry position using data supplied.
- Explain why a correlation between sugar consumption and type II diabetes does not establish cause.
- Identify two limitations of an animal study used as evidence about human diabetes.
- Describe how to produce a dilution series of a glucose solution, stating the volumes used at each step.
- Explain why the Benedict's solution must be in excess and why every tube must be heated for the same time.
- Use a calibration curve to determine the glucose concentration of an unknown sample and state the limits of that reading.
Marking Points
Key points examiners look for in your answers
- Absorption of glucose from the small intestine after a carbohydrate meal raises blood glucose concentration.
- Respiration of glucose by cells lowers blood glucose concentration, particularly during exercise.
- Glycogenesis in liver and muscle cells lowers blood glucose concentration by storing glucose as glycogen; insulin promotes this.
- Glycogenolysis in the liver raises blood glucose concentration by breaking down glycogen to glucose; both glucagon and adrenaline stimulate this process.
- Gluconeogenesis raises blood glucose concentration by making glucose from non-carbohydrate sources such as glycerol and amino acids; glucagon stimulates this process.
- Body mass is a risk factor for type 2 diabetes, not an acute factor controlling blood glucose concentration.
- Glycogenesis described as the conversion of glucose into glycogen for storage, lowering blood glucose concentration.
- Glycogenolysis described as the breakdown of glycogen into glucose, raising blood glucose concentration; AQA mark schemes accept the hydrolysis of glycogen.
- Gluconeogenesis described as the production of glucose from non-carbohydrate sources such as glycerol and amino acids.
- Glucose released by the liver enters the blood and becomes available for respiration by body cells.
- Each process linked to its hormonal control: insulin promotes glycogenesis; glucagon and adrenaline promote glycogenolysis, while glucagon also stimulates gluconeogenesis.
- Liver cells (hepatocytes) identified as the site of these processes; naming hepatocytes is creditworthy but not essential if liver cells are clearly indicated.
- Insulin is secreted by the beta cells of the islets of Langerhans when blood glucose concentration rises.
- Insulin attaches to specific receptors on the cell-surface membranes of target cells.
- The number of channel or transporter proteins in the membrane increases, so more glucose is taken up by facilitated diffusion.
- Enzymes are activated that catalyse the conversion of glucose into glycogen.
- The resulting fall in blood glucose concentration reduces insulin secretion, which is negative feedback.
- Glucagon is secreted by the alpha cells of the islets of Langerhans when blood glucose concentration falls.
- Glucagon attaches to receptors on the cell-surface membranes of liver cells, its target cells.
- Binding activates enzymes that catalyse the conversion of glycogen into glucose, which is glycogenolysis.
- Binding activates enzymes that catalyse the conversion of glycerol and amino acids into glucose, which is gluconeogenesis.
- Glucose leaves the liver cells and enters the blood, raising blood glucose concentration and reducing further glucagon secretion.
- Adrenaline attaches to specific receptors on the cell-surface membranes of target cells.
- Binding causes the activation of enzymes involved in the conversion of glycogen to glucose.
- In liver cells, glycogenolysis releases glucose into the blood, raising blood glucose concentration.
- In muscle cells, glycogenolysis provides respiratory substrate for rapid ATP production during stress or exercise.
- Adrenaline or glucagon binds to a specific receptor on the cell-surface membrane of a liver cell.
- The activated receptor stimulates adenylate cyclase, a membrane-bound enzyme.
- Adenylate cyclase catalyses the conversion of ATP into cyclic AMP.
- Cyclic AMP acts as a second messenger that activates protein kinase.
- Protein kinase initiates a cascade that activates enzymes, ending with glycogen phosphorylase, which breaks down glycogen; glucose-1-phosphate is produced and converted to glucose in liver cells.
- Amplification explained: one hormone molecule leads to many cAMP molecules and many activated enzyme molecules, so a low hormone concentration produces a large response.
- Type I caused by destruction of the beta cells of the islets of Langerhans, so little or no insulin is produced.
- People with type II diabetes still produce and release insulin, but target cells are less responsive or less sensitive to it.
- Type I controlled by insulin injections matched to diet and exercise; insulin is injected because it would be digested by proteases if swallowed.
- Type II controlled by manipulation of the diet, weight loss and exercise, with drugs or insulin added later if needed.
- Obesity and a diet high in fat and sugar identified as risk factors for type II diabetes, using the term risk factor rather than cause.
- Autoimmune destruction of beta cells described as the cause of type I diabetes.
- An argument supporting the health advisers' position that uses data or evidence supplied, for example linking a rise in sugar consumption or obesity to a rise in type II diabetes incidence.
- An argument supporting the food industry's position that uses data or evidence supplied, for example noting that many people with high sugar intake do not develop type II diabetes.
- An explicit statement that a correlation between diet and type II diabetes does not by itself establish causation, because other variables may be involved.
- A valid limitation of the evidence, such as the study being on animals rather than humans, too short to show long-term effects, or not controlling for genetics, age or inactivity.
- A justified conclusion that follows from the evidence discussed, for example that diet is likely to be one risk factor among several rather than the sole cause.
- Reference to at least one other risk factor for type II diabetes, such as genetics, ethnicity, age or inactivity, and an explanation of how it weakens a simple dietary explanation.
- Describe a valid dilution method, giving the volumes of stock solution and distilled water used for each concentration.
- Use an excess of Benedict's solution, with the same volume, temperature and time for every tube.
- Filter or centrifuge to remove the precipitate before taking the colorimeter reading.
- Plot absorbance, or transmission, against known glucose concentration to produce the calibration curve.
- Read the concentration of the unknown sample from the curve after treating it in exactly the same way.
Examiner Tips
Expert advice for maximising your marks
- 💡Split your answer into factors that raise blood glucose concentration and factors that lower it.
- 💡Distinguish the hormones carefully: insulin lowers glucose; glucagon raises glucose via glycogenolysis and gluconeogenesis; adrenaline raises glucose via glycogenolysis.
- 💡Mention body mass only as a risk factor for type 2 diabetes, not as an acute control mechanism.
- 💡Learn the three words by their endings: genesis makes it, lysis splits it, and gluconeogenesis makes new glucose from something that was not carbohydrate.
- 💡Always state the direction each process moves blood glucose concentration, and name the hormone that controls it, remembering glucagon stimulates both glycogenolysis and gluconeogenesis.
- 💡When explaining why liver glycogen but not muscle glycogen can raise blood glucose, refer to glucose-6-phosphatase in liver cells.
- 💡Use the phrase attaches to receptors on the cell-surface membrane, because that wording is the mark.
- 💡Two separate marks sit in insulin's action, more transporter proteins and activated enzymes; give both.
- 💡If the question concerns a diabetic patient, check whether the problem is insulin production or receptor sensitivity before writing.
- 💡Write glucagon and glycogen carefully; examiners cannot give the benefit of the doubt between the two.
- 💡Give both enzyme-activated processes, because the statement lists them separately and questions usually want both.
- 💡Mirror your insulin answer: same structure, opposite direction, different cells of the islets.
- 💡When describing adrenaline's action, explicitly state it binds to cell-surface receptors and activates enzymes, rather than acting directly.
- 💡Distinguish between liver cells (which release glucose into the blood) and muscle cells (which use the glucose internally for ATP production).
- 💡Learn the chain in order: hormone, receptor, adenylate cyclase, ATP to cAMP, protein kinase, glycogen phosphorylase, glucose-1-phosphate to glucose.
- 💡Say the words second messenger explicitly when you name cyclic AMP.
- 💡If asked why this system is efficient, answer with amplification: one hormone molecule leads to many glucose molecules released.
- 💡Set the answer out as a contrast, giving cause, age of onset and treatment for each type in turn.
- 💡Use the term risk factor rather than cause when discussing obesity and diet.
- 💡When evaluating data, comment on the species studied, sample size and duration of the study before drawing conclusions.
- 💡Structure the answer as for, against, therefore; ensure both sides are covered before writing the conclusion.
- 💡Quote figures from the table or graph rather than describing the pattern in words alone, and say what each figure shows.
- 💡State what further evidence would settle the question, such as a long-term controlled study on humans that accounts for genetics and lifestyle.
- 💡Name the control variables explicitly: volume and concentration of Benedict's solution, temperature, time and volume of sample.
- 💡State which axis is which, with known concentration on the x axis and absorbance on the y axis.
- 💡Benedict's test alone is only semi-quantitative; say that the colorimeter is what makes the result quantitative.
Common Mistakes
Pitfalls to avoid in your exam answers
- Listing only hormones and omitting diet and exercise. Correction: include absorption of glucose from the gut and respiration of glucose by cells.
- Confusing glycogenesis and glycogenolysis. Correction: genesis means making glycogen; lysis means splitting glycogen.
- Stating that adrenaline drives gluconeogenesis. Correction: adrenaline primarily stimulates glycogenolysis; glucagon stimulates both glycogenolysis and gluconeogenesis.
- Treating body mass as a direct acute control of blood glucose. Correction: body mass is a risk factor for type 2 diabetes, not an acute regulator.
- Mixing up the three terms, most often writing glycogenolysis when gluconeogenesis is meant. Correction: genesis makes it, lysis splits it, gluconeogenesis makes new glucose from non-carbohydrate sources.
- Claiming muscle glycogen can be released into the blood as glucose. Correction: muscle cells lack glucose-6-phosphatase, so muscle glycogen is used locally in respiration and cannot raise blood glucose.
- Stating that glucagon only stimulates gluconeogenesis. Correction: glucagon stimulates both glycogenolysis and gluconeogenesis.
- saying insulin converts glucose into glycogen itself, when it activates the enzymes that catalyse the conversion
- describing insulin as entering the target cell, when it attaches to a receptor on the outside of the membrane
- claiming glucose enters cells by active transport under insulin, when it is facilitated diffusion through channel proteins
- writing islets of Langerhans without specifying beta cells, when the question distinguishes the two cell types
- assuming insulin acts on every cell in the body equally, which ignores the idea of target cells with specific receptors
- Swapping alpha and beta cells, so glucagon is attributed to the wrong cells. Correction: glucagon is secreted by alpha cells; insulin by beta cells.
- Spelling glucagon as glycogen, or the reverse, which makes the answer unmarkable. Correction: glucagon is the hormone; glycogen is the storage polysaccharide.
- Saying glucagon breaks down glycogen directly rather than activating the enzymes that do so. Correction: glucagon activates enzymes such as glycogen phosphorylase.
- Claiming glucagon acts on muscle cells to release glucose into the blood. Correction: muscle lacks glucagon receptors and cannot release free glucose into the blood.
- Omitting gluconeogenesis, which is half of the specification statement. Correction: include both glycogenolysis and gluconeogenesis.
- Stating adrenaline hydrolyses glycogen; correction: adrenaline activates enzymes that catalyse phosphorolysis, not hydrolysis.
- Claiming muscle glycogenolysis raises blood glucose; correction: muscle cells lack the enzyme to release free glucose, so they use the breakdown products internally for respiration.
- Suggesting adrenaline enters the cell to act; correction: adrenaline binds to cell-surface receptors and acts via a second messenger system.
- Saying the hormone enters the cell and acts on the enzyme directly. Correction: the hormone is hydrophilic and binds to a cell-surface receptor; the second messenger carries the signal inside.
- Calling cyclic AMP the first messenger, or the hormone the second messenger. Correction: the hormone is the first messenger; cAMP is the second messenger.
- Writing that adenylate cyclase converts ADP or glucose into cyclic AMP. Correction: adenylate cyclase catalyses the conversion of ATP into cyclic AMP.
- Omitting protein kinase, so the chain jumps straight from cyclic AMP to glycogen breakdown. Correction: cAMP activates protein kinase, which phosphorylates further enzymes.
- Stating that glycogen phosphorylase hydrolyses glycogen directly to glucose. Correction: it catalyses phosphorolysis to glucose-1-phosphate, which is converted to glucose in liver cells.
- Saying people with type II diabetes produce no insulin. Correction: they still produce insulin, but target cells respond poorly to it.
- Claiming the pancreatic cells are destroyed in type II diabetes. Correction: beta cell destruction occurs in type I; type II involves insulin resistance.
- Writing that type I diabetes can be controlled by diet alone. Correction: type I requires insulin injections; diet and exercise are matched to the insulin dose.
- Treating a correlation between obesity and type II diabetes as proof that obesity causes it. Correction: obesity is a risk factor; correlation does not establish causation.
- Forgetting to explain why insulin cannot be taken as a tablet. Correction: insulin is a protein and would be hydrolysed by proteases in the digestive system.
- Writing an opinion piece that never refers to the data or evidence supplied. Correction: quote specific figures or findings from the table or graph in each paragraph.
- Giving only one side when the command word asks for an evaluation. Correction: structure the answer as for, against, therefore, covering both positions before concluding.
- Claiming that the data prove sugar causes type II diabetes. Correction: state that the data show a correlation, and that correlation does not establish causation.
- Dismissing a whole study because the sample was small, without explaining why this matters. Correction: explain that a small sample may not be representative, so conclusions cannot be generalised.
- Confusing a risk factor with a cause in the conclusion. Correction: describe diet as a risk factor that increases probability, not as a proven cause.
- Reading the colorimeter without removing the precipitate, so suspended solid scatters the light and the reading is unreliable. Correction: filter or centrifuge first.
- Heating tubes for different times or at different temperatures, which makes the comparison invalid. Correction: keep time and temperature constant for all tubes.
- Using too little Benedict's solution, so that it becomes limiting and all the high concentrations give the same reading. Correction: use excess Benedict's solution.
- Choosing the wrong filter, when a blue solution is read using a red filter because it absorbs red light. Correction: use a red filter for blue solutions.
- Extrapolating beyond the highest standard to read an unknown, instead of diluting the unknown into range. Correction: dilute the unknown so its reading falls within the calibration range.