How does the body manage glucose demand amid competing cortisol & insulin actions?

AI Thread Summary
Cortisol triggers gluconeogenesis in the liver, particularly in the morning, leading to increased glucose levels. The discussion centers on whether insulin production responds to this glucose rise, which could result in a cycle where the liver stores glucose as glycogen unnecessarily. If insulin does not respond, insulin-sensitive cells like skeletal muscle may lack GLUT4 expression, hindering glucose uptake. The relationship between cortisol-induced gluconeogenesis and insulin secretion is crucial for maintaining glucose supply to muscles while preventing futile glycogenesis in the liver. Clarifying how insulin response differs from dietary glucose, especially in the absence of GLP-1, is essential for understanding this metabolic balance.
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TL;DR Summary
How does the body behave in terms of insulin response due to cortisol induced gluconeogenesis?
Cortisol normally initiates gluconeogenesis especially in the mornings,

1. Glucose rises due to liver gluconeogenesis.
2. Does insulin production respond to this glucose rise?
3. If it entails insulin production (due to rise in glucose), liver might store it back as glycogen leading to a futile cycle.
4. If it does not entail insulin production, the other insulin sensitive cells such as skeletal muscle cells might suffer for want of GLUT4 expression and glucose uptake.

How does the body behave (in terms of insulin response) due to cortisol induced gluconeogenesis?

How does the body ensure supply of glucose to skeletal muscle cells at the same time ensuring liver does not undergo futile glycogenesis, due to insulin response?
 
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Here's a Nature article that reports that "glucagon stimulates gluconeogenesis".
In contrast, here is a PubMed article that reports that "glucocorticoids promote gluconeogenesis in liver".
The suggestion is that unlike glucagon that can trigger gluconeogenesis, glucocorticoids are just a contributing factor.
 
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Thanks. But my question is about the insulin secretion in response to the gluconeogenesis. How insulin response would be different for instance from dietary glucose? Obviously GLP-1 would be missing. Something like that.
 
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