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Why does insulin activate cholesterol synthesis whereas Glucagon and Epinephrine inhibit it?
I'm looking for the "global reason" (not like the biochemical path but just in general, why does that make sense)?
My hypothesis is:
Insulin is released in the fed state when the body has sufficient glucose (to make Acetyl-CoA and eventually, ATP). Thus, excess Acetyl-CoA can be used to make cholesterol (which is important for making bile acids, sterioids, etc.).
Glucagon/Epinephrine are released when there is a shortage of glucose and thus you don't want to "waste" the Acetyl-CoA on making cholesterol?
I know I'm probably wrong but can someone provide the real reason?
Also a second question: What is the reason for why thyroxine activates cholesterol synthesis?
I'm looking for the "global reason" (not like the biochemical path but just in general, why does that make sense)?
My hypothesis is:
Insulin is released in the fed state when the body has sufficient glucose (to make Acetyl-CoA and eventually, ATP). Thus, excess Acetyl-CoA can be used to make cholesterol (which is important for making bile acids, sterioids, etc.).
Glucagon/Epinephrine are released when there is a shortage of glucose and thus you don't want to "waste" the Acetyl-CoA on making cholesterol?
I know I'm probably wrong but can someone provide the real reason?
Also a second question: What is the reason for why thyroxine activates cholesterol synthesis?
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