Control of blood glucose concentration — AQA GCSE Biology

After a carbohydrate-rich meal, glucose absorbed from the small intestine raises the concentration of glucose in the blood plasma. The pancreas detects this rise and secretes insulin into the blood. Insulin travels to target cells, especially liver and muscle cells, and increases the rate at which they take up glucose from the blood. It does this by increasing the permeability of cell membranes to glucose, so glucose moves from the blood into the cells. Inside the cells, glucose is used in respiration or stored. As cells remove glucose from the blood, the blood glucose concentration falls back towards its normal set point, completing the negative feedback loop.

When insulin causes glucose to enter liver and muscle cells, not all of it is used immediately in respiration. Excess glucose is converted into glycogen, a large insoluble polysaccharide made from many glucose units joined together. Glycogen is stored in the liver and in muscle tissue and acts as a reserve of glucose. Storing glucose as glycogen is useful because glycogen is insoluble, so it does not affect the water potential of the cell and cannot diffuse out. When blood glucose concentration later falls, glucagon stimulates the breakdown of glycogen back into glucose, which is released into the blood. This storage and release cycle helps keep blood glucose concentration stable between meals.

To explain insulin control, describe a complete negative feedback sequence. After a meal, glucose absorbed into the blood raises blood glucose concentration. The pancreas detects this rise and secretes insulin into the blood. Insulin travels to liver and muscle cells and increases the permeability of their cell membranes to glucose, so glucose moves from the blood into the cells. Inside the cells, glucose is used in respiration and any excess is converted to glycogen for storage. As glucose leaves the blood, blood glucose concentration falls back towards its normal set point. When the concentration becomes too low, the pancreas secretes glucagon, which stimulates the breakdown of glycogen to glucose, raising blood glucose concentration again.

Insulin is the hormone released by the pancreas when blood glucose rises after a meal. It travels in the blood and causes liver and muscle cells to take up glucose and store it as glycogen, lowering blood glucose. In Type 1 diabetes the pancreatic cells that make insulin are damaged, so too little insulin is secreted. Without enough insulin, glucose stays in the blood instead of entering cells, producing the high blood glucose that characterises the disorder. Students should link cause to effect: pancreas failure means insufficient insulin, which means poor glucose uptake. A useful method is to trace the pathway pancreas → insulin → target cells → glucose uptake, then remove insulin and predict the consequence.

Because the pancreas of a person with Type 1 diabetes secretes insufficient insulin, glucose absorbed from the gut is not removed from the blood quickly enough. Blood glucose therefore rises after meals and is described as uncontrolled and high. Treatment replaces the missing hormone: insulin is injected, usually before meals, so that glucose can be taken up by liver and muscle cells and stored as glycogen. Insulin cannot be taken as a tablet because it is a protein and would be digested in the stomach. Students should be able to explain why injection is used and why the dose must be matched to food intake and activity.

In Type 2 diabetes the pancreas still produces insulin, but the body cells, particularly liver and muscle cells, become less responsive to it. This is often called insulin resistance. Because the signal is ignored, glucose is not taken up from the blood efficiently, so blood glucose remains high. The pancreas may initially secrete more insulin to compensate, but over time it can become exhausted. Students should contrast this clearly with Type 1: in Type 1 the pancreas cannot make enough insulin, whereas in Type 2 insulin is made but target cells respond poorly. Risk factors include obesity, poor diet and inactivity, though genetics also contribute.

Because Type 2 diabetes involves poor responsiveness to insulin, treatment often focuses on reducing the glucose load and improving how well cells respond. A carbohydrate controlled diet limits how much carbohydrate, especially sugar, is eaten, so smaller rises in blood glucose occur after meals. Regular exercise increases the rate at which muscles use glucose and can improve insulin sensitivity, helping cells respond better. Together these measures can lower blood glucose and, in some cases, reduce the need for medication. Students should explain the mechanism, not just list the treatments, and should link each treatment to its effect on blood glucose.

A risk factor raises the chance that a condition develops; it is not a guaranteed cause. Obesity means carrying excess body fat, often indicated by a high body mass index. In Type 2 diabetes, body cells respond poorly to insulin, so blood glucose stays too high. Excess fat tissue is linked to reduced insulin sensitivity, so the pancreas must release more insulin to have the same effect. Over time, this added demand can contribute to the development of Type 2 diabetes. For example, a person with a high BMI who eats an energy-rich diet and takes little exercise has a greater risk than someone of healthy mass who is physically active. Genetics and age also affect risk, so obesity is one factor among several.

Both types of diabetes produce high blood glucose, but their causes and treatments differ. In Type 1 diabetes, the pancreas produces little or no insulin, often because the insulin-secreting cells are damaged. Treatment involves injecting insulin, usually several times a day, and monitoring blood glucose and diet. In Type 2 diabetes, the pancreas still produces insulin but body cells respond less well to it. Treatment often begins with diet and exercise to reduce body mass and improve insulin sensitivity, and may include medicines that lower blood glucose. Some people with Type 2 diabetes eventually need insulin. Comparing the two means identifying the cause, typical age of onset, whether insulin is produced, and the main treatment approach.

After a meal, blood glucose rises and the pancreas releases insulin, which causes cells to take up glucose and the liver to store it as glycogen, so blood glucose falls. A graph may plot blood glucose concentration against time for a person without diabetes and a person with diabetes. To extract information, read values from the axes, identify the starting level, the peak after eating, and the time taken to return towards the starting level. To interpret, compare the two curves: the person without diabetes usually shows a smaller rise and a quicker return, while a person with diabetes may show a larger or more prolonged rise. Link each feature to insulin action, such as reduced insulin production or reduced sensitivity.

Blood glucose is controlled by negative feedback. When blood glucose falls too low, such as after exercise or between meals, the pancreas detects this and releases glucagon into the blood. Glucagon travels to liver cells and stimulates the breakdown of glycogen, a storage polysaccharide, into glucose. The glucose is released from liver cells into the blood, so blood glucose concentration rises back towards normal. This is an example of negative feedback because the response reverses the original change. Insulin and glucagon therefore have opposite effects: insulin lowers blood glucose, while glucagon raises it. The liver acts as the main store of glycogen and the key target organ for glucagon.

Blood glucose is controlled by two pancreatic hormones acting antagonistically in a negative feedback cycle. When blood glucose rises after a meal, insulin is secreted by the pancreas; it increases the rate at which glucose is taken up by cells and converted to glycogen in the liver and muscles, so glucose falls. When blood glucose falls, for example after fasting, glucagon is secreted; it stimulates the liver to break down glycogen into glucose, which is released into the blood, so glucose rises. Because each hormone reverses the change that triggered the other, the level oscillates around a set point. A useful method is to trace one loop: stimulus, receptor, hormone, effector (e.g. the liver), response, correction.