Lesson 3 of 4 / Cell signalling and glucose control
Insulin signals a fall in blood glucose
How does an extracellular hormone alter glucose uptake and storage?
In this lesson: Outline insulin signalling through a receptor tyrosine kinase.
About 7 min
The key ideaInsulin binding activates its membrane receptor pathway, promoting glucose uptake and storage through tissue-specific responses.
Explore the idea
Insulin: follow the signal to its effect
A rise in blood glucose stimulates pancreatic beta cells to secrete insulin. Choose a target tissue and predict its response.
Moving existing transporter-containing vesicles to the surface can increase uptake before total transporter protein increases. Glucose then enters by facilitated diffusion; insulin does not pump glucose across the membrane.
Original pathway schematic. Receptor shapes and intermediate numbers are simplified; the two receptor classes remain distinct. The feedback arrow means the corrected glucose deviation reduces the stimulus for secretion, not that glucose physically travels back along this drawn route. Other regulatory inputs are omitted.
Explanation
After a rise in blood glucose, pancreatic beta cells release insulin. Insulin binds a receptor tyrosine kinase on responsive cells, causing an activating conformational change and phosphorylation events that initiate downstream signalling.
In muscle and adipose cells, the pathway can increase the number of glucose transporters at the cell surface, increasing facilitated glucose uptake. In muscle and liver it promotes glycogen synthesis and favours storage over glucose release. Do not assume every tissue uses exactly the same transporter response.
These responses lower blood glucose towards its regulated range. As the initiating rise is reduced, insulin secretion decreases, completing negative feedback. Insulin is a signal; it is not itself an enzyme that converts glucose molecules into glycogen.
The required outline links ligand binding, receptor type, downstream signalling and physiological response. It does not require naming every intermediate kinase or messenger. In an experiment, failure of receptor activation can prevent a response even when insulin is present, separating signal supply from target-cell sensitivity.
Step by step
- 1
Name the trigger and source
A rise in glucose stimulates pancreatic beta cells.
- 2
Name the receptor event
Ligand binding initiates receptor-kinase signalling.
- 3
Connect to the feedback effect
Uptake and storage reduce the original rise.
Worked example
Work through the evidence
Insulin concentration rises, but a receptor-defective muscle cell does not increase surface glucose transporters. Explain.
One way to explain it
The ligand is present, but receptor signalling cannot initiate the downstream trafficking response, so the normal increase in facilitated uptake is impaired.
Why this answer works
- Hormone availability and cellular response are distinct.
- The transporter moves glucose; insulin communicates the signal.
Is this true? "Insulin lowers glucose by chemically digesting it in the blood."
It signals target cells to alter uptake and metabolism; cellular enzymes perform the reactions.