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Glucose: the body’s fuel
Glucose is a simple sugar, the fuel almost every cell prefers. Blood carries it to every cell. How much glucose the blood holds, called blood sugar, is kept inside a narrow healthy band.
The Lab / Core medicine / Lesson 13
Insulin and glucose.
After a carbohydrate-containing meal, sugar floods your blood, and in a healthy body it is back where it started within a few hours. Build up how insulin clears it, see the two ways diabetes breaks the loop, then watch six kinds of diabetes medicine each fix a different part.
Educational, not for clinical use
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A meal sends glucose into the blood
The gut breaks down carbohydrates, starchy and sugary foods such as bread, rice and fruit, into glucose and absorbs it into the blood. After a meal, blood sugar starts to climb. Something has to clear it again.
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The pancreas answers with insulin
The pancreas is an organ behind the stomach. Tiny clusters of cells in it, called islets, hold beta cells that sense rising blood sugar and release insulin, a hormone: a chemical messenger carried in the blood.
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The gut sends an early signal
Food in the gut also makes it release incretins, gut hormones that tell beta cells to release more insulin while blood sugar is rising. An enzyme, a protein that drives a chemical reaction, soon breaks incretins down.
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Insulin opens the doors
Muscle and fat cells are insulin’s main targets. When insulin docks on one, the cell moves glucose transporters, doorways for glucose, up to its surface, and glucose flows in to be burned or stored. Without insulin, few doors are open.
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The liver stores the extra
Insulin also tells the liver, the body’s chemical workshop, to stop releasing glucose and to pack the extra away as glycogen, a stored chain of glucose. Muscle stores some glycogen too.
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Back into the band, and insulin eases off
As glucose leaves the blood, blood sugar falls back into the band and the beta cells release less insulin. The result switches off its own cause. This is negative feedback, and it keeps blood sugar steady.
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Between meals, glucagon tops it up
Between meals and overnight, blood sugar starts to dip. Alpha cells in the islets then release glucagon, insulin’s opposite. It tells the liver to turn glycogen back into glucose and to make new glucose, topping the blood back up.
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The kidneys hand glucose back
The kidneys filter blood to make urine (Lesson 2), and glucose slips out with the filtered fluid. Pumps called SGLT2, short for sodium–glucose transporter 2, carry it back into the blood, so almost none is lost.
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Diabetes: when the loop fails
Diabetes mellitus is a lasting disease in which this loop fails and blood sugar stays too high, called hyperglycemia. It fails in two main ways: the body makes too little insulin, or cells stop answering it well.
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The whole picture: one key measure
Gut, pancreas, muscle, fat, liver and kidneys share the job: insulin lowers blood sugar, glucagon raises it. The key measure is blood sugar itself, often taken after an overnight fast and then called fasting blood sugar.
What changes it
Type 1 diabetes: no insulin
In type 1 diabetes the immune system, the body’s defence against germs, destroys the beta cells. Almost no insulin is made, so few doors open, the liver keeps releasing glucose and blood sugar climbs high, even before eating.
What changes it
Type 2 diabetes: cells stop answering
In type 2 diabetes, by far the most common kind, cells become insulin resistant: they answer insulin weakly. Beta cells release extra insulin to make up for it, but over time they tire out, and blood sugar stays high.
What changes it
Insulin injections: the missing hormone, from outside
Insulin injections put the hormone under the skin, since stomach acid would destroy it as a pill. It replaces what the beta cells no longer make: doors open again and the liver holds back glucose. In type 1 diabetes it is essential.
What changes it
Metformin: the liver makes less
Metformin, a tablet for type 2 diabetes, mainly cuts how much glucose the liver makes. It also helps cells answer insulin a little better and trims how much glucose the gut absorbs.
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Sulfonylureas: beta cells pushed harder
Sulfonylureas are tablets that bind to a switch on beta cells, a potassium channel, pushing them to release more insulin. They need beta cells that still work, and can drive blood sugar too low, called hypoglycemia.
What changes it
SGLT2 inhibitors: sugar leaves in urine
SGLT2 inhibitors are tablets that block the kidney’s glucose pumps. Filtered glucose is no longer carried back, so extra sugar leaves in the urine and blood sugar falls. Passing more urine is a common effect.
What changes it
GLP-1 receptor agonists: a stronger incretin signal
GLP-1 receptor agonists are drugs, usually injected, that act like GLP-1 (glucagon-like peptide 1), one of the gut’s incretins. When blood sugar is high they boost insulin release; they also limit glucagon and slow how fast the stomach empties.
What changes it
DPP-4 inhibitors: incretins last longer
DPP-4 inhibitors are tablets that block DPP-4 (dipeptidyl peptidase 4), the enzyme that breaks incretins down. The body’s own incretins last longer, so beta cells release more insulin when blood sugar is rising.
Step 1 of 19
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Reference values, beside the model.
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Normal teaching baseline.
The blue line on each bar is an illustrative teaching model, not a patient measurement; its readings, and the end points of each bar, are teaching-model choices, not reference values. The shaded bands are the reference ranges quoted under each row. Selecting a disease, drug or state shows the expected direction of each value from the cited passage. For a drug, the direction compares it with the untreated disease it is used for, and the model applies the drug to that disease.
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Run the meal yourself.
An illustrative teaching model of one meal. Pick a starting body, switch medicines on and off (they combine), and move the sliders. The dashed curve is the normal body; the solid curve is your settings.
Blood glucose over the hours after the meal (illustrative model)
How this teaching model works
Blood glucose changes each minute by what comes in minus what goes out. In: glucose absorbed from the meal (a smooth hump that peaks about half an hour after eating) and glucose released by the liver (raised by glucagon, held back by insulin). Out: a nearly steady uptake by the brain and other cells that do not need insulin; uptake into muscle and fat, proportional to insulin × how well cells answer it × glucose; and, above a carrying limit, glucose lost in the urine.
The beta cells release insulin along a steep curve of rising glucose, boosted by incretins from the gut (a small amount all the time, more after a meal). Insulin in the blood follows that release with a delay of minutes. Glucagon rises as glucose falls below the model’s fasting level and falls as glucose rises, within limits. Each run first settles overnight with no food, which gives the fasting level, and then the meal starts.
Each medicine moves the model in the direction of its cited mechanism: insulin adds insulin from outside the body (steady all day with an extra rise around the meal); metformin cuts liver glucose, trims gut absorption and slightly improves the response to insulin; a sulfonylurea pushes the remaining beta cells to release more insulin, partly whatever the glucose; an SGLT2 inhibitor lowers the level at which glucose spills into urine; a GLP-1 receptor agonist strengthens glucose-dependent insulin release, lowers glucagon and slows stomach emptying; a DPP-4 inhibitor strengthens the body’s own incretin signal. The sizes of all these effects are illustrative choices; only their directions are meant to teach.
Left out: fat and protein in the meal, exercise, stress hormones, the slow tiring of beta cells over years, ketones, and every real-world difference between people. The model’s fasting glucose is set inside the quoted reference range; nothing here is a prediction for a real person.