BLUEPRINTUNIT 4 · CELL COMMUNICATIONInteractive lab
RECEPTION → TRANSDUCTION → RESPONSE → FEEDBACK
Two hormones. One glucose balance.
Start with the feedback loop. Explore each hormone’s pathway, then bring them together to investigate blood-glucose regulation.
THE CENTRAL IDEAA response changes glucose.
Glucose changes the signal.
Glucose changes the signal.
Starting glucose
Feedback loop
Glucagon release
Pathway condition
Insulin release
Insulin response
Add a meal
Each tab keeps its own trial. Switching tabs pauses the experiment. Amounts and time are relative teaching units.
01 · SEE THE WHOLE LOOP
The response reduces the original stimulus.
Predict how glucose changes hormone release. Try low or high starting glucose, add a meal, and compare working with interrupted feedback.
Follow the hormones
60.0blood-glucose index
Below target
Below target
GGlucagonIInsulinGlucose
Particles illustrate hormone levels and glucose flow.
Does glucose return toward the target?
Blood-glucose indexTarget band · 95–105
READ THE LOOP
The dashed return path carries information about glucose. Its T-bar means recovery reduces the original stimulus.
02 · GLUCAGON
From low glucose to liver glucose release.
CED focus: reception, relay, amplification and response.
MOLECULAR VIEW
CED focus · Topics 4.2–4.4Liver cell · glucagon response
Swipe across the diagram to follow the pathway →
GlucagoncAMPPhosphate (P)Active enzyme
Protein shapes are based on experimental structures. Colours, movement and quantities are simplified teaching representations. Focus on what each component does.
Optional extension: inspect the experimental receptor models
Drag to rotate the Cα backbone model. Choose the active receptor–Gs complex (6LMK) or the aligned inactive receptor (5XEZ). Seven transmembrane regions are coloured; extracellular regions are blue-grey. Glucagon is amber and Gs subunits are blue, green and grey. The main diagram interpolates between receptor structures; that transition is illustrative, not an observed or calculated atomic trajectory.
View structure and primary publication at RCSB PDB ↗Low blood glucose→Pancreatic alpha cells→Glucagon release→Liver response
This trial starts at low glucose (60), with insulin release held off. Trace the G protein and cAMP relay in the model above.
03 · INSULIN
A different receptor. A different cellular response.
INSULIN RESPONSE · MUSCLE / FAT CELL
A different receptor · a different responseInsulin receptor → glucose uptake
Insulin binds its receptor and triggers a relay that brings more glucose transport proteins to the membrane. Glucose then enters by facilitated diffusion.
Swipe across to follow insulin and glucose →
InsulinGlucoseTransport protein
The receptor and relay here are simplified teaching diagrams. Surface and reserve counts sum to a fixed pool of 20 model transporters. Sustained maximum insulin stimulation gradually recruits all 20 in the normal condition; Auto may reduce the signal before this happens. Glucose movement through a transporter is facilitated diffusion; insulin does not carry or pump glucose through the membrane.
High blood glucose→Pancreatic beta cells→Insulin release→Muscle / fat uptake
This trial starts near the target (100). Run it and add a small, medium or big meal: watch glucose rise, insulin bind and more transporters reach the membrane. Glucagon is held off to isolate the insulin response; this trial isolates one pathway rather than full whole-body regulation.
04 · WORKING TOGETHER
One blood-glucose level. Two coordinated responses.
GLUCAGON · LIVER
Glucagon secretion: 0%Release glucose
From this glycogen pathway 0.00Background liver production 0.00relative glucose units / model s
INSULIN · MUSCLE / FAT
Insulin secretion: 0%Take up glucose
The whole-body diagram and total liver-output readout include both sources. Insulin also reduces background liver production.
CELL RESPONSES → WHOLE-BODY FEEDBACK
Connect the cell responses to feedback
One shared glucose pool
60.0blood-glucose index
Below target
Below target
GGlucagonIInsulinGlucose
Particles illustrate hormone levels and glucose flow.
Follow the glucose, then the signal.
As liver release raises low glucose, the stimulus for glucagon release decreases. As uptake lowers high glucose, the stimulus for insulin release decreases.
The hormones act through different pathways. Their effects meet at the shared blood-glucose pool. Blue glucose particles show release and uptake; the dashed return path shows feedback.
Teacher notes · assumptions and sources
Learning focus: AP Biology CED Topics 4.2–4.4: reception, transduction, cellular response and negative feedback. This is a qualitative teaching model; values are arbitrary indices, not clinical blood-glucose measurements.
Experiments: each tab preserves an independent trial. Changing a starting-glucose, feedback or insulin-condition button starts a fresh, paused trial. Hormone On / Off switches act during a trial; existing hormone and downstream effects take time to fade. Feedback interrupted holds Auto release at the initial glucose stimulus. Isolated pathway tabs hold the other hormone off.
Glucagon: the model condenses GPCR → Gs → adenylyl cyclase → cAMP → PKA → kinase cascade → glycogen breakdown. The finite glycogen store is not replenished. Optional molecular details and structures are extensions beyond required pathway naming.
Insulin: its receptor tyrosine kinase activates a condensed relay that recruits GLUT4 to muscle and fat cell membranes. Glucose enters by facilitated diffusion, while cellular processing maintains an inward gradient. Surface plus reserve transporters always total 20. Relative receptor activation is scaled so that sustained maximum model insulin gives 100% activation and approaches 20 surface transporters in the normal condition; this is an illustrative scale, not a measured transporter count or the percentage of receptors bound. Resistance reduces this relative response. Basal uptake continues without insulin. The insulin-only trial also includes other tissue use but switches off liver glucose replacement, so blood glucose can keep falling without a meal. The first and last tabs include liver glucose production. The cellular-use animation follows the model’s combined processing of glucose for respiration or storage; it does not assign an ATP yield or separate storage and respiration quantities.
Insulin resistance: insulin can bind, but receptor-to-cell signalling is reduced to 12% of the normal response in this illustrative condition. This represents one possible signalling defect; insulin resistance can also involve downstream processes. No insulin production represents loss of beta-cell insulin release, a simplified type 1 diabetes condition. Type 2 diabetes may involve both insulin resistance and insufficient insulin production.
Whole-body balance: the first and last tabs also include ongoing liver glucose production from other substrates, suppressed by insulin signalling. It is accounted for separately from the finite glycogen store. This allows comparison of glucose recovery when insulin responses are impaired. Small, medium and big meals add 20, 40 and 60 relative glucose units, absorbed smoothly over 20, 25 and 30 model seconds. Meals are also available in the isolated insulin trial, which starts near the target. These are illustrative carbohydrate loads, not dietary or clinical quantities. Additional meals add to the current trial; reset clears them. Exercise, other hormones, renal glucose loss and long-term adaptations are omitted. The normal reference uses the same initial conditions, meal inputs and model time.
Particle interpretation: secretion badges refer to new pancreatic hormone release. Circulating hormone and downstream responses decay gradually. The compact liver pathway's blue particles use only its glycogen-derived output; background production is reported separately. No particles leave this pathway when its glucose output is zero.
Sources: AP Biology course framework · Glucagon receptor–Gs complex · Insulin receptor · Insulin signalling and GLUT4 recruitment · Hepatic glucose production · Insulin resistance · Type 1 diabetes.