Blood Sugar, Stress & Diabetes

Describe the hormones, then analyse the disease. The second half depends on the first, because diabetes is best explained as the failure of a mechanism you have just set out.

6 marks: about two for the blood-glucose pair, one for the stress hormones, and the rest for diabetes and its effect on homeostasis. Name each hormone, its source and its effect.

Insulin, secreted by the pancreas, lowers blood glucose: when glucose rises after a meal, insulin causes body cells to take up glucose from the blood and causes the liver to store the surplus as glycogen. Glucagon, also secreted by the pancreas, raises blood glucose: when glucose falls, it causes the liver to break glycogen down and release glucose into the blood.

Together insulin and glucagon form a negative feedback pair operating around a set point. A rise above the set point triggers insulin, whose effect is to lower glucose; a fall below it triggers glucagon, whose effect is to raise it. Each response opposes the change that triggered it, so blood glucose is held within a narrow range regardless of when the person last ate.

The primary stress hormones are adrenaline and cortisol. Adrenaline, secreted rapidly by the adrenal medulla, produces the immediate fight-or-flight response, increasing heart rate and breathing rate and raising blood glucose to make energy available at once. Cortisol, secreted more slowly by the adrenal cortex, sustains that state during prolonged stress, maintaining raised blood glucose over a longer period. Both therefore raise blood glucose, but on different timescales.

Diabetes disrupts this control at the insulin step. In Type 1 diabetes the immune system destroys the insulin-producing cells of the pancreas, so little or no insulin is made. In Type 2 diabetes insulin is still produced, but the body's cells become resistant to it and respond poorly. In both cases the effect is the same: glucose cannot be taken up and stored properly, so it accumulates in the blood, a condition called hyperglycaemia.

Because the insulin arm of the feedback pair cannot act, blood glucose is not returned to its set point after a meal and remains elevated. Homeostasis is lost, not because the body has stopped detecting the change, but because the effector response that opposes it is unavailable. The immediate consequences follow from the excess glucose: it exceeds the kidney tubule's maximum reabsorption rate and is excreted in the urine, drawing water osmotically with it and causing thirst and frequent urination. Over years, persistently high blood glucose damages blood vessels, nerves, kidneys, eyes and the heart. Treatment — insulin injections in Type 1, and diet, exercise and medication in Type 2 — restores artificially the control the body has lost.

Analyse data means describing the trends and then interpreting them, with every claim supported by a figure from the table. An interpretation that could have been written without the data will not earn the data marks.

5 marks. Describe each trend using the numbers, compare the two, attribute the difference to insulin, and conclude about homeostasis.

Person A starts at 5 mmol/L, rises to a peak of 8 at 30 minutes, falls to 6 by 60 minutes, and is back to 5 at 120 minutes. The pattern is a rise following the glucose drink and a complete return to the starting value within two hours.

Person B starts at 9 mmol/L, which is already above Person A's starting value, rises to 15 at 30 minutes and continues rising to a peak of 16 at 60 minutes, then falls only slightly to 14 at 120 minutes — still well above the starting value and far above Person A's. Three features distinguish this trend: a raised fasting level, a larger rise, and a peak that occurs later and is never cleared.

In Person A, the rise in blood glucose triggers insulin secretion, and insulin causes body cells to take up glucose and the liver to store it as glycogen, which is what returns the level to 5 mmol/L within two hours. In Person B the same rise occurs but the corrective fall does not, which indicates that insulin action is impaired — either because too little is produced, as in Type 1 diabetes, or because cells respond poorly to it, as in Type 2. Since both people received the same glucose dose, the difference lies in the response to the rise rather than in the size of the challenge.

The data therefore illustrate insulin's regulating role by showing what happens in its absence. Person A demonstrates homeostasis working: a variable disturbed from its set point is detected and returned to it by an opposing response. Person B demonstrates its failure: the variable is disturbed, no effective opposing response occurs, and it remains outside the normal range two hours later. A raised fasting value of 9 mmol/L further indicates that the failure is chronic rather than a one-off, since blood glucose has not been restored even before the test began. This is why a glucose-tolerance test is diagnostic — it measures not the peak but whether the return happens.