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Old 01-20-2015
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Default regulation of F2,6BP by unsulin

I'm kind of confused by the mechanism by which insulin regulates glycolysis and gluconeogensis by it's effect on Fructose 2,6 Bisphosphate.

Which of the two is it? by action of cAMP? or by action of IRS----SH2----protein phosphatase?
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Old 01-20-2015
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The explanation is,

Glucagon and Insulin are opposite in nature,glucagon increases blood sugar levels by causing glycogen breakdown while insulin causes glycogen synthesis...

in short insulin is always anabolic while glucagon is catabolic

Insulin by itself has nothing to do with cAMP levels so if you say Insulin decreases cAMP levels then you are wrong...

While Glucagon has direct corelation to cAMP...ie increased glucagon levels means increased cAMP means the protein kinase A will be activated and hence the enzyme will get phosphorylated and breakdown Fructose 2,6-bisphosphate to Fructose 6-phsophate....and as glucagon is high during low blood sugar levels so this is the case of Neoglucogenesis

When during glycolysis, an ANABOLIC process insulin is high and glucagon is low, then since glucagon is low cAMP levels are low, so the enzyme is actually less phosphorylated due to abscence of protein kinase a due to relative lack of glucagon...

Now you may ask so what is there to do for INSULIN, insulin in this case acts by different mechanism like you said IRS----SH2----protein phosphatase and will inactivate the already activated(phosphorylated) enzyme...

IN SHORT:

*Glucagon acts by increasing cAMP
*Insulin acts by de-phosphorylation (protein phsophatase)

*Lack of glucagon means low cAMP means no more new phosphorylation of the enzyme
*Presence of insulin means removal of phosphate group from already activated enzyme

Insulin acts via protein phosphatase always and has nothing to do with cAMP levels directly,absence of glucagon does...


Hope I didnt confuse you too much
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Quote:
Originally Posted by CleverFOX View Post
The explanation is,

Glucagon and Insulin are opposite in nature,glucagon increases blood sugar levels by causing glycogen breakdown while insulin causes glycogen synthesis...

in short insulin is always anabolic while glucagon is catabolic

Insulin by itself has nothing to do with cAMP levels so if you say Insulin decreases cAMP levels then you are wrong...

While Glucagon has direct corelation to cAMP...ie increased glucagon levels means increased cAMP means the protein kinase A will be activated and hence the enzyme will get phosphorylated and breakdown Fructose 2,6-bisphosphate to Fructose 6-phsophate....and as glucagon is high during low blood sugar levels so this is the case of Neoglucogenesis

When during glycolysis, an ANABOLIC process insulin is high and glucagon is low, then since glucagon is low cAMP levels are low, so the enzyme is actually less phosphorylated due to abscence of protein kinase a due to relative lack of glucagon...

Now you may ask so what is there to do for INSULIN, insulin in this case acts by different mechanism like you said IRS----SH2----protein phosphatase and will inactivate the already activated(phosphorylated) enzyme...

IN SHORT:

*Glucagon acts by increasing cAMP
*Insulin acts by de-phosphorylation (protein phsophatase)

*Lack of glucagon means low cAMP means no more new phosphorylation of the enzyme
*Presence of insulin means removal of phosphate group from already activated enzyme

Insulin acts via protein phosphatase always and has nothing to do with cAMP levels directly,absence of glucagon does...


Hope I didnt confuse you too much


Nope, you didn't confuse me at all, thanx for taking the time to explain thoroughly.

I thought the same as you said BUT what confused me is in my FA (2014 edition) p.102 says that increased insulin leads to decreased cAMP and decreased Kinase A which was contradictory to what kaplan said!

thanx alot
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