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Control of blood glucose concentration Q Watch

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    My (OCR) textbook says that "in response to a high blood glucose concentration, the Beta-cells secrete insulin which binds to receptors on the hepatocytes. This activates adenyl cyclase inside each cell which converts ATP to cAMP. The cAMP activates a series of enzyme-controlled reactions in the cell (e.g. glycogenesis).

    However, for a low glucose concentration, it simply says "the alpha-cells secrete glucagon. Its target cells are hepatocytes which possess the specific receptor for glucagon. The effects of glucagon include glycogenolysis etc...)

    Does this mean that the action of glucagon does not involve conversion of ATP to cAMP and that the reactions in the cell to bring about glycogenolysis do not involve cAMP??

    Thanks.
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    I would assume ATP is converted to cAMP because glycagon remember is a protein hormone, it cannot go into the cell itself to bring about effects like glycogenolysis. Therefore, it needs a secondary messenger substance to do that- which is cAMP.
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    (Original post by BethMay17)
    My (OCR) textbook says that "in response to a high blood glucose concentration, the Beta-cells secrete insulin which binds to receptors on the hepatocytes. This activates adenyl cyclase inside each cell which converts ATP to cAMP. The cAMP activates a series of enzyme-controlled reactions in the cell (e.g. glycogenesis).

    However, for a low glucose concentration, it simply says "the alpha-cells secrete glucagon. Its target cells are hepatocytes which possess the specific receptor for glucagon. The effects of glucagon include glycogenolysis etc...)

    Does this mean that the action of glucagon does not involve conversion of ATP to cAMP and that the reactions in the cell to bring about glycogenolysis do not involve cAMP??

    Thanks.
    I'm no expert in this but from what I've learned in Bio, I think that you may have muddled the role of insulin with adrenaline. Adrenaline is used to increase the glucose concentration similar to glucagon where as insulin is used to lower the glucose concentration.

    From my understanding, adrenaline uses the second messenger model to activate an enzyme to convert ATP into cAMP as you mentioned before. I do not think that insulin is involved in the second messenger model as it stimulates a glucoprotein channel to open after binding to a specific receptor. This allows the glucose to diffuse into the cell and be used up in glycogenesis. Adrenaline also inhibits the release of insulin and stimulates the further release of glucagon.

    Glycogenolysis can occur via adrenaline or glucagon. When glucagon is involved there is no cAMP. If glycogenolysis occurs due to adrenaline then yes cAMP is involved as it's the second messenger.

    Hope this helps
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    (Original post by pinkcalculator23)
    I'm no expert in this but from what I've learned in Bio, I think that you may have muddled the role of insulin with adrenaline. Adrenaline is used to increase the glucose concentration similar to glucagon where as insulin is used to lower the glucose concentration.

    From my understanding, adrenaline uses the second messenger model to activate an enzyme to convert ATP into cAMP as you mentioned before. I do not think that insulin is involved in the second messenger model as it stimulates a glucoprotein channel to open after binding to a specific receptor. This allows the glucose to diffuse into the cell and be used up in glycogenesis. Adrenaline also inhibits the release of insulin and stimulates the further release of glucagon.

    Glycogenolysis can occur via adrenaline or glucagon. When glucagon is involved there is no cAMP. If glycogenolysis occurs due to adrenaline then yes cAMP is involved as it's the second messenger.

    Hope this helps
    For an OCR past paper question ("Describe how negative feedback is used to control blood glucose concentration", the mark scheme says

    AVP; 11 e.g. correct cellular detail for insulin release or in effector cells …
    ● insulin binds to receptor on plasma membrane of hepatocytes
    ● correct ref to secondary messenger (cAMP) e.g. ref to inhibitory effect(s) of hormone …
    ● conversion in cells / secretion of antagonist

    However it doesn't mention anything about glucagon and cAMP?
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    (Original post by BethMay17)
    For an OCR past paper question ("Describe how negative feedback is used to control blood glucose concentration", the mark scheme says

    AVP; 11 e.g. correct cellular detail for insulin release or in effector cells …
    ● insulin binds to receptor on plasma membrane of hepatocytes
    ● correct ref to secondary messenger (cAMP) e.g. ref to inhibitory effect(s) of hormone …
    ● conversion in cells / secretion of antagonist

    However it doesn't mention anything about glucagon and cAMP?


    Glucagon and cAMP aren't directly related to each other. Although they have similar roles as they both stimulate glycogenolysis, glucoagon doesn't stimulate the release of cAMP as that is the function of cAMP.

    What you have to remember is that glucagon is a hormone and cAMP is formed from ATP. One is a protein and the other is formed from an energy releasing molecule.

    Although they have similar roles in increasing glucose concentration the manner they do so is completely different. Glucagon can be released into the blood and get to work where as adrenaline needs to be released first, ATP needs to be converted into cAMP and then a series of reactions are stimulated to eventually increased glucose concentration- there are many more steps in the process when cAMP is involved compared to glucagon


    Negative feedback mechanisms is all about opposing x change and maintaining it back to the normal level. Looking at your mark scheme, insulin is mentioned to show an understanding that this is the hormone released when the glucose concentration gets too high. cAMP will inhibit any further release of insulin, after being adrenaline binds to the receptor to stimulate its formation from ATP. The glucose can now be converted to glycogen in cells if glucose levels are too high/glycogen is converted to glucose when glucose levels are too low.

    Mark schemes give you the basic outline/skeleton of what your answer needs but doesn't always give you the example or model answer which is needed. Remember mark schemes are part of the tick list that examiners use to award marks and your answer is likely to have more detail than the 3 bullet points in their marks scheme.

    Hope this helps, if you need any help let me know
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    (Original post by pinkcalculator23)

    cAMP will inhibit any further release of insulin, after being adrenaline binds to the receptor to stimulate its formation from ATP.
    Thanks for your help

    Looking at someone else's revision notes on F214, I have seen it said that a fall in blood glucose concentration inhibits insulin production. Is this what you were talking about with the role of cAMP? Does the cAMP stop insulin production while glucagon raises glucose levels (by glycogenolysis?)
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    (Original post by BethMay17)
    Thanks for your help

    Looking at someone else's revision notes on F214, I have seen it said that a fall in blood glucose concentration inhibits insulin production. Is this what you were talking about with the role of cAMP? Does the cAMP stop insulin production while glucagon raises glucose levels (by glycogenolysis?)
    Yes, if your glucose concentration is decreasing, you want to stop it decreasing any further otherwise you will become hypoglacaemic. The insulin is inhibited.
    Glucagon is stimulated so to raise the glucose concentration. cAMP does play a part in this when adrenaline is involved but remember adrenaline is only used when your body is under immense pressure/stress or there's a dangerously low level of glucose in the blood, glucagon is the primary hormone used otherwise as your first line of defence/port of call. The glucagon will inhibit insulin so that glycogenolysis can occur.

    If you need any more help, just ask
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    (Original post by pinkcalculator23)
    The glucagon will inhibit insulin so that glycogenolysis can occur.
    It's tempting to assume that, but there is evidence to suggest glucagon actually stimulates insulin production in the pancreas rather than inhibiting it (I don't know if that's an indirect effect though). I doubt the OP will need to know that, though - just thought I'd throw that out there.
 
 
 
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