Homeostasis – A-Level Biology Revision Notes

In negative feedback, a change away from the set point triggers a response that reverses the change and restores the original level – this is how most homeostatic systems work. In positive feedback, a change triggers a response that amplifies the original change, moving the system further from the set point. Positive feedback is much less common in the body but does occur, for example in the release of oxytocin during childbirth and in the depolarisation phase of an action potential.

When blood glucose rises, the beta cells of the islets of Langerhans in the pancreas secrete insulin. Insulin binds to receptors on liver and muscle cells, increasing the number of glucose-transporter channel proteins in their membranes so they take up more glucose. It also activates the enzymes that convert glucose to glycogen (glycogenesis) and increases the rate of respiration. Together these lower the blood glucose back to its set point.

Glycogenesis is the conversion of glucose into glycogen for storage, promoted by insulin. Glycogenolysis is the breakdown of glycogen back into glucose, promoted by glucagon and adrenaline. Gluconeogenesis is the production of new glucose from non-carbohydrate sources such as glycerol and amino acids, also promoted by glucagon. The names are easy to mix up, so it helps to read them carefully: -genesis means making, -lysis means breaking, and gluconeo- means new glucose.

Filtration happens by ultrafiltration in the glomerulus. Blood enters through a wide afferent arteriole and leaves through a narrower efferent arteriole, creating high hydrostatic pressure. This forces small molecules – water, glucose, ions and urea – out of the blood and into the Bowman’s capsule, forming the glomerular filtrate. Large molecules such as plasma proteins and blood cells are too big to pass through and remain in the blood. Useful substances are then reabsorbed further along the nephron.

When the water potential of the blood falls (dehydration), osmoreceptors in the hypothalamus detect the change and the posterior pituitary gland releases more ADH. ADH makes the walls of the collecting duct more permeable to water by inserting aquaporins, so more water is reabsorbed into the blood and a small volume of concentrated urine is produced. When the body is over-hydrated, less ADH is released, less water is reabsorbed, and a large volume of dilute urine is produced. This is negative feedback restoring the water potential to its set point.

The second messenger model explains how glucagon and adrenaline act on cells. The hormone (the first messenger) binds to a receptor on the cell surface, which activates the enzyme adenylate cyclase. Adenylate cyclase converts ATP into cyclic AMP (cAMP), the second messenger. cAMP then activates protein kinase enzymes inside the cell, which catalyse glycogenolysis to release glucose. This model is required by AQA and OCR A.

When the body is too cold, the hypothalamus coordinates several responses: vasoconstriction reduces blood flow near the skin surface so less heat is lost; sweat production decreases; the hair erector muscles contract so hairs stand up and trap an insulating layer of air; shivering (rapid muscle contraction) releases heat from increased respiration; and the metabolic rate can be raised (for example by thyroxine) to generate more heat. These responses reduce heat loss and increase heat production until core temperature returns to normal.

In Type I diabetes, the beta cells of the pancreas cannot produce insulin, usually because of an autoimmune response, so blood glucose cannot be lowered after a meal. It is controlled by injecting insulin. In Type II diabetes, the beta cells still produce insulin, but the target cells become less responsive to it because their receptors lose sensitivity. It is strongly linked to diet, obesity and age, and is usually controlled by managing diet and increasing exercise. Knowing the cause of each type is a common exam requirement.