Glucose is the fuel your cells respire, so you cannot afford to run out. It is also a small soluble molecule, so too much of it in the blood drags water out of your cells by osmosis. Your body therefore has to keep it in a narrow band — and it does that with two hormones that pull in opposite directions.
📚 What you need to know
Blood glucose is controlled by negative feedback and kept within narrow limits.
The islets of Langerhans in the pancreas contain two cell types: α cells secrete glucagon, β cells secrete insulin.
Insulin lowers blood glucose: cells take up glucose, and liver and muscle store it as glycogen (glycogenesis).
Glucagon raises blood glucose: liver glycogen is hydrolysed back to glucose (glycogenolysis), and amino acids can be converted to glucose (gluconeogenesis).
Type 1 diabetes — the β cells are destroyed by an autoimmune response, so too little insulin is made.
Type 2 diabetes — insulin is still made, but target cells stop responding to it (insulin resistance).
Both types raise blood glucose, causing glucose in the urine, large urine volumes, thirst and fatigue.
Why glucose has to be controlled
Two separate problems force the body to keep blood glucose steady.
Glucose is the substrate for respiration. If the concentration drops too low, cells — especially brain cells — cannot make enough ATP.
Glucose is soluble. Dissolved glucose lowers the water potential of the blood. Too much of it and water is drawn out of the surrounding cells by osmosis, so the osmotic balance between cells and blood is disturbed.
The pancreas: two jobs in one organ
Most of the pancreas is exocrine tissue that makes digestive enzymes and releases them into a duct. Scattered through it are small patches of endocrine tissue called the islets of Langerhans, which release hormones straight into the blood.
Cell type
Hormone secreted
Secreted when…
Overall effect
β (beta) cells
Insulin
blood glucose rises
lowers blood glucose
α (alpha) cells
Glucagon
blood glucose falls
raises blood glucose
🧠
Beta is for “banking it”
Beta cells make insulin, which banks the glucose away as glycogen. Alpha cells do the opposite. And glucagon has an a in it, like alpha.
The loop in full
This is the same three-part loop from the last page. The receptors and the effectors happen to be in the same organ: the islet cells detect the change and secrete the hormone that corrects it.
Read down one column at a time. Notice that the receptor and the effector for this loop live in different places: the islet cells detect and secrete, but the liver does the actual storing and releasing.
What insulin actually does
Insulin is secreted by the β cells when blood glucose rises. It travels in the blood to target cells all over the body, mainly in the liver and muscles, and binds to receptors on their cell surface membranes. Four things follow.
Glucose channels open in the cell surface membranes, so glucose moves out of the blood into cells by facilitated diffusion.
Liver and muscle cells convert the excess glucose into glycogen for storage. This is glycogenesis.
The rate of respiration increases, using glucose up.
Some glucose is converted into fatty acids and stored as fat.
What glucagon actually does
Glucagon is secreted by the α cells when blood glucose falls, for example after fasting or exercise. Its main target is the liver.
It activates enzymes that hydrolyse glycogen back into glucose, which then enters the blood. This is glycogenolysis.
It causes amino acids to be converted into glucose. This is gluconeogenesis, which literally means “making new glucose”.
The rate of respiration decreases, so less glucose is used up.
Three words that look the same
Glycogenesis = making glycogen • Glycogenolysis = splitting glycogen (lysis) • Gluconeogenesis = making new glucose from something else
Glucagon and glycogen are one letter apart and examiners see them swapped constantly. Glucagon is the hormone. Glycogen is the storage polysaccharide. If your sentence says “the pancreas releases glycogen”, you have lost the mark.
What this looks like after a meal
The dip after the peak surprises students, but it is exactly what negative feedback predicts: insulin acts until glucose is back in range, by which point a little too much has been stored, so glucagon takes over.
Diabetes
Diabetes is the condition in which homeostatic control of blood glucose has failed or deteriorated. In both types, insulin no longer works properly, so glucose concentration in the blood rises and stays high.
The shared symptoms, and why they happen
Glucose in the urine. The kidneys cannot reabsorb all of the extra glucose from the filtrate, so some is excreted.
Large volumes of urine, and thirst. The glucose left in the filtrate lowers its water potential, so less water is reabsorbed. The person loses water and becomes dehydrated.
Fatigue. Glucose stays in the blood instead of entering cells, so the rate of respiration is reduced and less ATP is made.
Organ damage if blood glucose reaches dangerously high levels after meals.
Type 1
Type 1 diabetes usually begins in childhood. An autoimmune response causes the person’s own immune system to attack the β cells of the islets of Langerhans. Once those cells are damaged, insulin production can no longer take place, so blood glucose cannot be lowered.
It is managed with regular blood tests, insulin injections (particularly after meals) and a modified diet with reduced carbohydrate intake.
Type 2
Type 2 is more common and usually develops in older adults. Here the pancreas still makes insulin, but the receptors on the cell surface membranes that insulin binds to have reduced in number or no longer respond. This is insulin resistance.
The pancreas compensates by secreting more and more insulin, but eventually it cannot keep up. Glucose uptake falls and blood glucose stays high. Obesity is a major risk factor: over-production of insulin in response to a consistently high-carbohydrate diet triggers the development of resistance.
It is managed with medication to lower blood glucose, a low-carbohydrate diet (rapidly digested foods cause dangerous spikes) and an exercise regime.
Type 1
Type 2
Cause
Pancreas is unable to produce enough insulin
Body cells become resistant to insulin
Insulin level in blood
Low or absent
Normal or high, at least at first
Typical onset
Childhood
Older adults
Treatment
Monitoring blood glucose and injecting insulin, especially after meals
Low-carbohydrate diet and regular exercise, with medication if needed
The distinguishing question. If you are given data and asked which type of diabetes a patient has, look at their insulin level, not their glucose level. High glucose with low insulin points to type 1. High glucose with normal or high insulin points to type 2.
Worked examples
WE 1
Explaining a return to normal
A person’s blood glucose concentration rises from 5.0 mmol dm−3 to 8.4 mmol dm−3 after a meal, and returns to 5.2 mmol dm−3 two hours later. Explain how the fall is brought about. (4 marks)
Step 1: detection
The rise is detected by the β cells of the islets of Langerhans in the pancreas.
Step 2: the hormone
These cells secrete insulin, which is transported in the blood to target cells in the liver and muscles.
Step 3: the effect on the cells
Glucose channels open, so glucose enters cells by facilitated diffusion, and the rate of respiration increases.
Step 4: storage
Excess glucose is converted to glycogen in liver and muscle cells (glycogenesis), lowering the concentration in the blood.
Beta cells → insulin → uptake → glycogenesisthe rise of 3.4 mmol dm−3 is not needed for the marks, but quoting figures never hurts.
WE 2
Identifying the type of diabetes
Two patients are tested two hours after a glucose drink. Patient P has a blood glucose of 12.0 mmol dm−3 and a blood insulin concentration of 8 pmol dm−3. Patient Q has a blood glucose of 11.6 mmol dm−3 and a blood insulin concentration of 190 pmol dm−3. A healthy person would have around 90 pmol dm−3. Deduce which type of diabetes each patient has, giving reasons. (4 marks)
Step 1: what both share
Both have blood glucose well above the normal range, so in both, glucose is not being taken up by cells.
Step 2: patient P
P’s insulin is far below the healthy value, so the pancreas is not producing enough. This is type 1, caused by autoimmune destruction of the β cells.
Step 3: patient Q
Q’s insulin is above the healthy value, yet glucose is still high, so the target cells are not responding to it. This is type 2, caused by insulin resistance.
Step 4: explain Q’s high value
The pancreas is secreting extra insulin to try to compensate for the reduced response of the cells.
Read the insulin column, not the glucose column“deduce” means use the data. Quote both numbers in your answer.
WE 3
Why glucagon still matters at rest
Explain why a person’s blood glucose concentration does not fall to zero overnight, when no food is eaten for ten hours. (3 marks)
Point 1: detection
The falling concentration is detected by the α cells, which secrete glucagon into the blood.
Point 2: the main effect
Glucagon activates enzymes in liver cells that hydrolyse stored glycogen into glucose, which is released into the blood (glycogenolysis).
Point 3: the backup effect
Amino acids can also be converted into glucose (gluconeogenesis), and the rate of respiration decreases so less glucose is used.
Stored glycogen is the overnight fuel tanka nice extra: this is also why a long run makes you feel wobbly — the glycogen store eventually runs low.
💡 Exam tips
Spell out the full chain: detected by β cells → insulin secreted → taken up by liver and muscle → stored as glycogen.
Name the cells (α or β) and the tissue (islets of Langerhans). “The pancreas” alone is often not enough.
Insulin causes facilitated diffusion, not active transport, of glucose into cells.
Check spellings before you hand the paper in: glucagon, glycogen, glycogenesis, glycogenolysis, gluconeogenesis.
When a graph shows insulin and glucose together, describe them in relation to each other — insulin rises after glucose rises, not at the same time.
⚠ Common mistakes
Writing that the pancreas releases glycogen. It releases glucagon. Glycogen is stored in the liver.
Saying insulin breaks down glucose. It causes uptake and storage; respiration breaks glucose down.
Saying type 2 diabetics produce no insulin. They do — often more than usual. Their cells stop responding.
Saying eating sugar causes type 1. Type 1 is autoimmune. Diet is a risk factor for type 2, not type 1.
Forgetting the muscles. Insulin’s target cells are in the liver and muscles, not the liver alone.
Saying the liver detects blood glucose. The islet cells detect it; the liver is the effector.
Up next: Thermoregulation. Same loop, different factor. This time the receptors are in your skin and your hypothalamus, and the effectors include blood vessels, sweat glands, tiny hair muscles and your entire metabolic rate.
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