Epinephrine is not a neurotransmitter...

[MCAT guy]

I believe I learned that it was both a hormone and a NT. But I got a BR question wrong because it can't be a NT?

Even though epinephrine increases insulin secretion from the pancreas (by stimulating its β2 adrenergic receptors), it too is considered a hormone, so we can eliminate choice B.

Elevated levels of glucose in the blood plasma trigger the release of insulin from the pancreas. The neurotransmitter directly responsible for insulin release is....

Acetylcholine

Is all this factual?

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[lorenzomicron]

epinephrine is definitely also an NT. however, i'm not sure about the specific action but it does regulate glucose via adrenergic receptors; it doesnt act when glucose is high.

 

[PiBond]

it's a neurohormone

 

[MCAT guy]

Some BR bio is strange in a bad way.

I just looked up on wikipedia:

Epinephrine (also known as adrenaline) is a hormone and neurotransmitter.[1]

source:

1. ^ Berecek KH, Brody MJ (1982). "Evidence for a neurotransmitter role for epinephrine derived from the adrenal medulla". Am J Physiol 242 (4): H593-601. PMID 6278965. edit

That's about 28 years ago they figured this out. Were the BR CBTs written before this?

 

[UIUCstudent]

I believe I learned that it was both a hormone and a NT. But I got a BR question wrong because it can't be a NT?





Is all this factual?

Why would epinephrine stimulate insulin? Isn't it more of a flight or fight hormone so you want the cell to take up glucose for energy? I'm a bit confused by the answer key as well.

 

[npparikh90]

idk what wikipedia says but epinephrine is released by the adrenals so hence its just a hormone. It nor-epinephrine that is a neurotransmitter/neurohormone.

 

[Hah]

I think its talking about it in context. Epinephrine primarily is a hormone when it comes to systemic activity. It has an extremely minor role in the CNS and has no role in the PNS. Norepinephrine is a main NT for the PNS, specifically for the sympathetic division.

The question here is what NT causes the release of insulin and the correct answer is indeed acetylcholine. The parasympathetic division of the PNS responsible for rest and ruminate/digest utilizes acetylcholine only whereas the sympathetic utilizes both acetylcholine and norepinephrine (norepinephrine when the efferent axons terminate at the organs and acetylcholine before it converges at the sympathetic ganglia).

I think the book is probably saying epinephrine ISN'T a NT with regards to the secretion of insulin. It acts as a hormone with regards to the secretion of sinulin

 

[banner18]

It acts as a hormone with regards to the secretion of sinulin

Epi.= Epinephrine
Ace.= Acetylcholine

NorEpi. actually inhibits insulin, and Epi. stimulates insulin (in fight/flight) but blood glucose is the primary stimulant for insulin. Ace. is the another possible way for insulin to be released. BTW, would the release of insulin be considered a parasympathetic response?

Lets say you face a flight vs. flight stimulus, the body would want to keep insulin high but wouldnt it also need to keep glucagon levels high to break down glycogen for extra energy? According to wikipedia in fight/flight insulin is inhibited (someone explain this.. i know that nor epi. inhibits it but adrenaline stimulates it both of which are in the sympathetic system)?? and glucagon is stimulated(makes sense to increase blood glucose) but dont you need insulin to have the muscles take in the glucose???

 

[PiBond]

Epi.= Epinephrine
Ace.= Acetylcholine

NorEpi. actually inhibits insulin, and Epi. stimulates insulin (in fight/flight) but blood glucose is the primary stimulant for insulin. Ace. is the another possible way for insulin to be released. BTW, would the release of insulin be considered a parasympathetic response?

Lets say you face a flight vs. flight stimulus, the body would want to keep insulin high but wouldnt it also need to keep glucagon levels high to break down glycogen for extra energy? According to wikipedia in fight/flight insulin is inhibited (someone explain this.. i know that nor epi. inhibits it but adrenaline stimulates it both of which are in the sympathetic system)?? and glucagon is stimulated(makes sense to increase blood glucose) but dont you need insulin to have the muscles take in the glucose???

Epinephrine released (in response to fight/flight) from the adrenal medulla will cause glycogen breakdown (in addition to gluconeogenesis) in the liver to provide glucose to the entire body at large. High amounts of glucose in the body trigger the release of insulin.

Norepi does inhibit insulin release via alpha-2 receptors, yet adrenaline (epi) stimulates insulin release via beta-2 receptors. In the end, insulin must be present for muscle cells to uptake glucose so the adrenaline mechanism of action predominates.

Hope that makes sense.

 

[Hah]

Epinephrine released (in response to fight/flight) from the adrenal medulla will cause glycogen breakdown (in addition to gluconeogenesis) in the liver to provide glucose to the entire body at large. High amounts of glucose in the body trigger the release of insulin.

Norepi does inhibit insulin release via alpha-2 receptors, yet adrenaline (epi) stimulates insulin release via beta-2 receptors. In the end, insulin must be present for muscle cells to uptake glucose so the adrenaline mechanism of action predominates.

Hope that makes sense.

Actually, I'm fairly certain that Norepinephrine/Epinephrine's binding on all four adrenergic receptors result in higher blood glucose and lower insulin levels. NEITHER stimulates insulin, rather, both inhibit and lower it.

Muscle actually does not need insulin during fight or flight. The purpose of insulin is to build up the glycogen stores in muscle during rest/ruminate (PNS periods) so that when fight or flight does occurs the glycogen stores in the muscles are ready to go. Blood glucose is reserved for other more important organs, namely the brain. Muscle also revert to fatty acid metabolism as soon as its glycogen stores run low.


So to summarize:

-Epinephrine= Adrenaline

-Both epinephrine and norepinephrine act to INCREASE BLOOD SUGAR and glucose metabolism by INHIBITING insulin and INCREASE IN GLUCAGON.

-Epinephrine and norepinenphrine do this by differing mechanisms. Epinephrine does this through a hormonal mechanism while Norepinephrine is released as a neurotransmitter.

 

[banner18]

Actually, I'm fairly certain that Norepinephrine/Epinephrine's binding on all four adrenergic receptors result in higher blood glucose and lower insulin levels. NEITHER stimulates insulin, rather, both inhibit and lower it.

that does not make any sense and is why im confused. why would the body increase blood glucose if it cant be taken into the tissues, insulin is the only way for glucose to enter any organ including the brain. therefore you must have insulin + glucagon in a sympathetic response. if you read up on epi. and norepi. you'll see that they activate diff. receptors to stimulate or inhibit insulin. I think what happens is norepi., cortisol and other glucocorticoids initially inhibit insulin so blood glucose can build up, then epi. and high glucose levels triggers insulin so that the glucose and be used in the body. it makes sense because after a stressful event blood glucose levels are waaay low and this is why gatorade/ sports drinks are useful.

oh and by the way you need glucose in order have anaerobic respiration, glucose is converted to pyruvate and lactic acid... the lack of glycogen or glucose in the muscle cells inst what triggers anaerobic resp. its the inability for the body to deliver enough O2 that makes aerobic ineffective during strenuous exercise.

 

[banner18]

in conlusion i aggree with PiBond haha

 

[jphwki82]

Epinephrine does the following:

1. Supresses pancreatic insulin release
2. Increases pancreatic glucagon relaease
3. Increases lipolysis
4. Increases glycogen breakdown
5. Enhances hepatic gluconeogenesis
6. Decreases glucose uptake by muscle & adipose, which makes more glucose available for the brain

Hormones that have an anti-insulin effects include epinephrine, glucagon, cortisol and growth hormone. Keep in mind that there is still insulin in the blood stream, it doesn't completely shut down. The insulin:glucagon ratio shifts. Sympathetic stimulation is inhibitor of insulin secretion too. Somatostatin is inhibitory to insulin secretion as well.

Things that will stimulate beta cell secretion of insulin are the following:

1. Nutrients = Glucose, Amino Acids & Fatty Acids
2. Hormones = Incretins, GLP-1, GIP
3. Ach from vagal parasympathetics
4. Rx = Sulfonylureas, Meglitinides & Incretin Analogs

 

[PiBond]

Epinephrine does the following:

1. Supresses pancreatic insulin release
2. Increases pancreatic glucagon relaease
3. Increases lipolysis
4. Increases glycogen breakdown
5. Enhances hepatic gluconeogenesis
6. Decreases glucose uptake by muscle & adipose, which makes more glucose available for the brain

Hormones that have an anti-insulin effects include epinephrine, glucagon, cortisol and growth hormone. Keep in mind that there is still insulin in the blood stream, it doesn't completely shut down. The insulin:glucagon ratio shifts. Sympathetic stimulation is inhibitor of insulin secretion too. Somatostatin is inhibitory to insulin secretion as well.

Things that will stimulate beta cell secretion of insulin are the following:

1. Nutrients = Glucose, Amino Acids & Fatty Acids
2. Hormones = Incretins, GLP-1, GIP
3. Ach from vagal parasympathetics
4. Rx = Sulfonylureas, Meglitinides & Incretin Analogs

I started to read a bit more and found that epinephrine does cause so-called "insulin resistance".

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC371414/

This contradicts the wikipedia article I had read previously about epinephrine stimulating insulin secretion.

 

[Hah]

that does not make any sense and is why im confused. why would the body increase blood glucose if it cant be taken into the tissues, insulin is the only way for glucose to enter any organ including the brain. therefore you must have insulin + glucagon in a sympathetic response. if you read up on epi. and norepi. you'll see that they activate diff. receptors to stimulate or inhibit insulin. I think what happens is norepi., cortisol and other glucocorticoids initially inhibit insulin so blood glucose can build up, then epi. and high glucose levels triggers insulin so that the glucose and be used in the body. it makes sense because after a stressful event blood glucose levels are waaay low and this is why gatorade/ sports drinks are useful.

oh and by the way you need glucose in order have anaerobic respiration, glucose is converted to pyruvate and lactic acid... the lack of glycogen or glucose in the muscle cells inst what triggers anaerobic resp. its the inability for the body to deliver enough O2 that makes aerobic ineffective during strenuous exercise.

Look it up. Norepi/Epi does not stimulate insulin in ANY manner on any receptor. During rest/ruminate periods your muscles are saturated, by use of insulin, with glycogen stores so that it is available during fight/flight. When in the event those glycogen stores are not enough it goes to fatty acid metabolism because blood glucose is reserved for the brain (which gets priority). Also, the brain DOES NOT need insulin to take in glucose. The only tissue that do are the liver/muscle/fat cells. The reason they use insulin is to build up a reservoire of glycogen so that it can be utilized during a sympathetic response.

Also your statement about gatorade is not entirely correct. The reason why gatorade helps after strenuous exercise is not because it provides sugar (if that were true soda would do the trick but you drinking soda isn't exactly helpful after stress now is it?) it is because it helps restore the electrolytes that can be lossed through sweat and urine.

 

[Hah]

I started to read a bit more and found that epinephrine does cause so-called "insulin resistance".

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC371414/

This contradicts the wikipedia article I had read previously about epinephrine stimulating insulin secretion.

Which wiki article did you read? The one that I found in no way states your previous claims:

"Adrenaline is a nonselective agonist of all adrenergic receptors, including α1, α2, β1, β2, and β3 receptors.[8] Epinephrine's binding to these receptors triggers a number of metabolic changes. Binding to α-adrenergic receptors inhibits insulin secretion by the pancreas, stimulates glycogenolysis in the liver and muscle, and stimulates glycolysis in muscle.[9] β-Adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland, and increased lipolysis by adipose tissue. Together these effects lead to increased blood glucose and fatty acids, providing substrates for energy production within cells throughout the body."

from http://en.wikipedia.org/wiki/Epinephrine

Also, here is the wiki page for adrenergic receptors and the two receptors that mitigate insulin (alpha-2 and beta-2) activity both inhibit/lower it:

http://en.wikipedia.org/wiki/Adrenergic_receptor#.CE.B11_receptor

 

[PiBond]

Which wiki article did you read? The one that I found in no way states your previous claims:

"Adrenaline is a nonselective agonist of all adrenergic receptors, including α1, α2, β1, β2, and β3 receptors.[8] Epinephrine's binding to these receptors triggers a number of metabolic changes. Binding to α-adrenergic receptors inhibits insulin secretion by the pancreas, stimulates glycogenolysis in the liver and muscle, and stimulates glycolysis in muscle.[9] β-Adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland, and increased lipolysis by adipose tissue. Together these effects lead to increased blood glucose and fatty acids, providing substrates for energy production within cells throughout the body."

from http://en.wikipedia.org/wiki/Epinephrine

Also, here is the wiki page for adrenergic receptors and the two receptors that mitigate insulin (alpha-2 and beta-2) activity both inhibit/lower it:

http://en.wikipedia.org/wiki/Adrenergic_receptor#.CE.B11_receptor

Straight from wikipedia article about insulin:

The sympathetic nervous system (via α2-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 β2-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 α2-receptors, then subsequently, circulating adrenaline from the adrenal medulla will stimulate β2-receptors thereby promoting insulin release.

 

[UIUCstudent]

Epinephrine does the following:

1. Supresses pancreatic insulin release
2. Increases pancreatic glucagon relaease
3. Increases lipolysis
4. Increases glycogen breakdown
5. Enhances hepatic gluconeogenesis
6. Decreases glucose uptake by muscle & adipose, which makes more glucose available for the brain

Hormones that have an anti-insulin effects include epinephrine, glucagon, cortisol and growth hormone. Keep in mind that there is still insulin in the blood stream, it doesn't completely shut down. The insulin:glucagon ratio shifts. Sympathetic stimulation is inhibitor of insulin secretion too. Somatostatin is inhibitory to insulin secretion as well.

Things that will stimulate beta cell secretion of insulin are the following:

1. Nutrients = Glucose, Amino Acids & Fatty Acids
2. Hormones = Incretins, GLP-1, GIP
3. Ach from vagal parasympathetics
4. Rx = Sulfonylureas, Meglitinides & Incretin Analogs

Awesome. Thanks for the bullet points. So just getting a little confused with this discussion. Norepinephrine and epinephrine can act as hormones and neurotransmitters (for the sympathetic)?

 

[Hah]

Straight from wikipedia article about insulin:

The sympathetic nervous system (via α2-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 β2-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 α2-receptors, then subsequently, circulating adrenaline from the adrenal medulla will stimulate β2-receptors thereby promoting insulin release.

The beauty of wikipedia is its contradictory information... sigh. That being said I can not find another source that supports those claims and the wiki passage did not cite where it got the information from. I'm going to some more digging and try to clarify this mass of information.

Edit:

http://diabetes.diabetesjournals.org/content/27/5/550.abstract

So I was wrong for asserting no stimulation is caused by epinephrine. Apparently according to the American Diabetes Association, epinephrine does cause slight stimulation however, inhibition is its dominating effect. So the post by jphwki82 probably best describes it. It's a shift in the circulating levels, insulin is probably never at a non detectable level in the body.

However, with that said it is important to note that insulin is secondary to the glycogen stores available in the muscle and that is where the muscle get its primary energy supply during fight or flight. The higher glucose blood level is for the the other organs, primarily the brain that DOES NOT need insulin to absorb glucose. The brain is ALWAYS number one in allocating available glucose.

 

[PiBond]

The beauty of wikipedia is its contradictory information... sigh. That being said I can not find another source that supports those claims and the wiki passage did not cite where it got the information from. I'm going to some more digging and try to clarify this mass of information.

Agreed. I found some academic articles supporting both epi/norepi decreasing insulin secretion so I'm going with those. Wikipedia loses a few cool points in my book though...

 

[banner18]

However, with that said it is important to note that insulin is secondary to the glycogen stores available in the muscle and that is where the muscle get its primary energy supply during fight or flight. The higher glucose blood level is for the the other organs, primarily the brain that DOES NOT need insulin to absorb glucose. The brain is ALWAYS number one in allocating available glucose.

OK I've been doing a lot of reading since this topic has been bugging me. In fight/flight, insulin is down-regulated via epi. but glucose is still able to enter the brain because it contains the GLUT2 receptor. GLUT2 is a passive transmembrane protein that passively shuttles glucose, its found in the liver and also in the hypothalamus/cerebrum AKA no insulin required for glucose to enter this cell as you said. Keep in mind though, that glucose cannot cross the blood-brain barrier by itself as your last two sentences imply, the GLUT2 allows glucose into the brain when insulin is not present. This itself answered my big question; why the heck would the body would increase blood glucose levels yet at the same time inhibit/ down-regulate insulin.

Its true that the brain requires nearly twice as much glucose as any other organ since A) it cant store its own glycogen and b) it is constantly metabolically active, especially during fight/flight. However, I dont know if your claims about insulin being secondary in mucsle to glycogen are necessarily true. You are right that muscle muscle glycogen is the primary source of ATP for the cell, but what happens when the glycogen stores are depleted? Note that the liver holds nearly 90% of the glycogen in the body, so muscles do not have enough glycogen for a continued stressful event.

Once the glycogen in the muscle has depleted in the form of pyruvate, ATP and in the case of an oxygen debt, lactic acid, the muscle MUST use blood glucose or else it will not function. The only way its getting this blood glucose is through insulin. Therefore, at some point, insulin must dominate to deliver glucose to skeletal muscle and vital organs (besides the brain which apparently can function without insulin).

I agree with you about gatorade and electrolytes but you cannot deny that strenuous exercise depletes sugar levels. Have you ever watched the ironman competition or some parts of a marathon? They drink gatorade mid-race to not only replenish electroyltes but the glucose serves as an immediate source of energy for muscle. In fact, i read a paper that said glucose in sports drinks are absorbed into the blood stream almost as quickly as an IV because the glucose is in single-chain carbs. I also know this because i work in a kinesiology lab... Do a VO2 max test and compare your blood glucose before and after. Its much lower, why? When the blood sugar levels drop due to the strenuous exercise, glucagon becomes activated (temporarily inhibiting insulin to prevent hypoglycemia) to break down the carbs and raise blood glucose. Then once again insulin dominates to ensure that the body does not become hyperglycemic and provides tissues with glucose for fuel.

the way I see it in fight or flight, insulin is initially inhibited due to norepi. and epi. and glucagon is expressed. Then, at some point insulin must predominate to shuttle glucose into the muscle because it cannot last on its own supply of glycogen. it needs glucose to function and the only way its going to get it is through insulin, if it does not get an adequate glucose supply you will probably fall right before the end of a marathon or right before youre able to escape that wild saber tooth tiger.

sorry to the OP since the last few posts by me are way off topic! to answer your question, ace. is purely an NT while epi. can act as both. They are only looking for a substance that is a NT, not a neurohormone like Epi. Its a really nitpicky Q&A that probs wont show up on the mcat..