Glucagon and Insulin: Let's straighten this out once and for all

[aashkab]

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Two very intertwining hormones that can be confusing at times, and I think the NBME likes to exploit it, so lets straighten this out because I've seen tons of inconsistencies from the sources I've used.

Glucagon -

1. promotes gluconeogenesis (via fructose 2, 6 bisphosphatase)
2. promotes glycogenolysis (via phosphorylation of glycogen phosphorylase kinase)
3. inhibits glycogen synthase
4. promotes insulin secretion (IS THIS RIGHT? I saw it somewhere and wrote it down)



Insulin -

From FA -
1. increases glucose transport
2. increases glycogen synthesis/storage
3. increases triglyceride synthesis/storage
4. increases cellular uptake of K+
5. increase protein synthesis
6. increases sodium retention (don't really know how this happens)

Not in FA -

7. Inhibits Glucagon


I'm really disappointed at the lack of glucagon emphasis in FA. It deserves its own half page at least. Anyways, if you guys can please see what is right /wrong and add your own idea of what the heck is going, it'd help out. I'm mainly very unsure of the INTERACTION between the two. I thought for a while they both inhibited each other, now it seems like only insulin inhibits.

Thanks!

 

[vr123]

Two very intertwining hormones that can be confusing at times, and I think the NBME likes to exploit it, so lets straighten this out because I've seen tons of inconsistencies from the sources I've used.

Glucagon -

1. promotes gluconeogenesis (via fructose 2, 6 bisphosphatase)
2. promotes glycogenolysis (via phosphorylation of glycogen phosphorylase kinase)
3. inhibits glycogen synthase
4. promotes insulin secretion (IS THIS RIGHT? I saw it somewhere and wrote it down)



Insulin -

From FA -
1. increases glucose transport
2. increases glycogen synthesis/storage
3. increases triglyceride synthesis/storage
4. increases cellular uptake of K+
5. increase protein synthesis
6. increases sodium retention (don't really know how this happens)

Not in FA -

7. Inhibits Glucagon


I'm really disappointed at the lack of glucagon emphasis in FA. It deserves its own half page at least. Anyways, if you guys can please see what is right /wrong and add your own idea of what the heck is going, it'd help out. I'm mainly very unsure of the INTERACTION between the two. I thought for a while they both inhibited each other, now it seems like only insulin inhibits.

Thanks!

Yes, glucagon stimulates a little insulin release because insulin-dependent tissues need it to take up glucose. If glucagon makes a whole lot of glucose via glycogenolysis, gluconeogeneis, etc but there isn't any insulin around, then the glucose won't be able to get into the cells. So that's why this seemingly contradictory effect occurs.

 

[XRanger]

yea i believed glucagon promotes insulin release to prevent wide fluctuation or glucose level getting too high.

insulin also promotes acetyl-coa carboxylase which leads to increased malonyl coa

 

[knuckles]

Insulin is a dephosphorylator (works via Tyrosine Kinase)

Glucagon is a phosphorylator (works via cAMP/PKA)

 

[sswang00]

yeah this was confusing the hell out of me too.

Another thing that Im a bit mixed up on is adrenergic effects on insulin/glucagon release. I had some conflicting info between DIT, UW, and FA. I am completely lost on this..

According to UWorld
alpha2 receptors - stim Glucagon release
beta receptors - increase Insulin release (not sure if they mean b1 or b2)

First Aid
alpha2 receptors - decrease insulin release (due to Glucagon??)
beta2 receptors - increase glucagon release (wth?!)

Then I dont know what the hell the DIT guy was trying to say..something along the lines of "its easy to remember because alpha stim beta cells of pancreas(insulin) and beta stimulates alpha cells of pancreas(glucagon)"



so yeah...wtff??
I don't know if im just an idiot but I cant seem to make sense of all this

 

[knuckles]

yeah this was confusing the hell out of me too.

Another thing that Im a bit mixed up on is adrenergic effects on insulin/glucagon release. I had some conflicting info between DIT, UW, and FA. I am completely lost on this..

According to UWorld
alpha2 receptors - stim Glucagon release
beta receptors - increase Insulin release (not sure if they mean b1 or b2)

First Aid
alpha2 receptors - decrease insulin release (due to Glucagon??)
beta2 receptors - increase glucagon release (wth?!)

Then I dont know what the hell the DIT guy was trying to say..something along the lines of "its easy to remember because alpha stim beta cells of pancreas(insulin) and beta stimulates alpha cells of pancreas(glucagon)"



so yeah...wtff??
I don't know if im just an idiot but I cant seem to make sense of all this

a2 decrease insulin
b2 increase insulin

Stop overcomplicating things

 

[aashkab]

yeah this was confusing the hell out of me too.

Another thing that Im a bit mixed up on is adrenergic effects on insulin/glucagon release. I had some conflicting info between DIT, UW, and FA. I am completely lost on this..

According to UWorld
alpha2 receptors - stim Glucagon release
beta receptors - increase Insulin release (not sure if they mean b1 or b2)

First Aid
alpha2 receptors - decrease insulin release (due to Glucagon??)
beta2 receptors - increase glucagon release (wth?!)

Then I dont know what the hell the DIT guy was trying to say..something along the lines of "its easy to remember because alpha stim beta cells of pancreas(insulin) and beta stimulates alpha cells of pancreas(glucagon)"



so yeah...wtff??
I don't know if im just an idiot but I cant seem to make sense of all this

yo swang, me too

but i eventually stuck with FA. B2 increases glucagon and insulin. A2 inhibits insulin.

 

[knuckles]

Another random thing you guys should know.

The mechanism behind glucagon being used as an antidote for B-blocker overdose, is that it increases cAMP. Simply put.

 

[aashkab]

Yes, glucagon stimulates a little insulin release because insulin-dependent tissues need it to take up glucose. If glucagon makes a whole lot of glucose via glycogenolysis, gluconeogeneis, etc but there isn't any insulin around, then the glucose won't be able to get into the cells. So that's why this seemingly contradictory effect occurs.

Is this also the case for excess cortisol, NE, and Epi?

I've seen conflicting things as well that NE and Epi inhibit insulin release but that doesn't make sense to me. Esp given the fact you have gluconeogenesis and the B2 receptor being activated with Epi. Not sure about NE

 

[aashkab]

from wiki:
The sympathetic nervous system (via Alpha2-adrenergic stimulation as demonstrated by the agonists clonidine or methyldopa) inhibit the release of insulin. However, it is worth noting that circulating adrenaline will activate Beta2-Receptors on the Beta cells in the pancreatic Islets to promote insulin release. This is important since muscle cannot benefit from the raised blood sugar resulting from adrenergic stimulation (increased gluconeogenesis and glycogenolysis from the low blood insulin: glucagon state) unless insulin is present to allow for GLUT-4 translocation in the tissue. Therefore, beginning with direct innervation, norepinephrine inhibits insulin release via alpha2-receptors, then subsequently, circulating adrenaline from the adrenal medulla will stimulate beta2-receptors thereby promoting insulin release.

finally, resolution, lol