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    Q: What are the major target tissues/organs of insulin? Summarize briefly the PROCESSES controlled by insulin action on: liver, skeletal muscle, adipose (fat) tissue

    I know that insulin targets the liver to store glucose as glycogen (so the process is glycogenesis), but I’m stuck on the muscle/fat tissue. I know that GLUT4 remains in vesicles until insulin causes them to fuse with the plasma membrane and allow glucose into the cell, but what would the answer to the ‘processes’ question be? Thanks in advance
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    (Original post by KUO101)
    Q: What are the major target tissues/organs of insulin? Summarize briefly the PROCESSES controlled by insulin action on: liver, skeletal muscle, adipose (fat) tissue

    I know that insulin targets the liver to store glucose as glycogen (so the process is glycogenesis), but I’m stuck on the muscle/fat tissue. I know that GLUT4 remains in vesicles until insulin causes them to fuse with the plasma membrane and allow glucose into the cell, but what would the answer to the ‘processes’ question be? Thanks in advance
    the process is a negative feedback loop, so when blood glucose levels increase insulin lowers blood glucose levels. i have no idea if this is the correct answer~~
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    The PROCESSES mentioned by OP are correct - other processes affected by insulin include:-

    1. It slows down the process of gluconeogenesis [Greek neo = new; genesis = production] - gluconeogenesis is the production of new glucose from amino acids (mainly) - slowing of this process obviously tends to lower blood glucose.

    2. Insulin slows down glycogenolysis [opposite of glycogenesis: Greek lyse = breakdown as in lysosome, which is the organelle where acid hydrolases break down internal [e.g. dead mitochondria] or external [e.g. phagocytosed bacteria] waste]. Less decomposition of glycogen into glucose, once again, reduces blood glucose.

    3. Increases protein synthesis in ribosomes

    4. Increases ketone uptake (this explains the classical diagnostic smell of hyperglycaemic coma patient due to increased levels of e.g. alphaketobutyrate)

    5. (In adipose tissue): - a) Activates lipoprotein lipase
    b) Increases fatty acid synthesis

    6. Increases K+ uptake in muscle and adipose tissue

    An additional fact to remember is that the opposite(s) of these actions are brought about by the hormones that are called insulin antagonists, namely adrenaline, corticosteroids and thyroxine - hence one less common cause of secondary diabetes is e.g. Cushing's syndrome.

    Hope this helps.

    M (ex-medic)
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    (Original post by macpatelgh)
    The PROCESSES mentioned by OP are correct - other processes affected by insulin include:-

    1. It slows down the process of gluconeogenesis [Greek neo = new; genesis = production] - gluconeogenesis is the production of new glucose from amino acids (mainly) - slowing of this process obviously tends to lower blood glucose.

    2. Insulin slows down glycogenolysis [opposite of glycogenesis: Greek lyse = breakdown as in lysosome, which is the organelle where acid hydrolases break down internal [e.g. dead mitochondria] or external [e.g. phagocytosed bacteria] waste]. Less decomposition of glycogen into glucose, once again, reduces blood glucose.

    3. Increases protein synthesis in ribosomes

    4. Increases ketone uptake (this explains the classical diagnostic smell of hyperglycaemic coma patient due to increased levels of e.g. alphaketobutyrate)

    5. (In adipose tissue): - a) Activates lipoprotein lipase
    b) Increases fatty acid synthesis

    6. Increases K+ uptake in muscle and adipose tissue

    An additional fact to remember is that the opposite(s) of these actions are brought about by the hormones that are called insulin antagonists, namely adrenaline, corticosteroids and thyroxine - hence one less common cause of secondary diabetes is e.g. Cushing's syndrome.

    Hope this helps.

    M (ex-medic)
    Insulin doesn't stimulate uptake of ketones. Insulin inhibits hormone-sensitive lipase (HSL) in adipocytes, therefore low levels of insulin lead to activation of HSL, causing free fatty acids to be released into the blood. These free fatty acids undergo beta-oxidation to form acetyl CoA which would normally enter the Krebs cycle/TCA cycle. However, as you've said, insulin inhibitis gluconeogenesis; therefore low levels of insulin stimulate gluconeogenesis, causing intermediates in the TCA cycle (such as oxaloacetate) to enter the gluconeogenic pathway to produce glucose. The depletion of these intermediates necessary for the TCA cycle inhibits the TCA cycle. Instead of the acetyl CoA entering the TCA cycle, it is converted to ketone bodies instead (beta-hydroxybutyrate, acetoacetate, and acetone), which can be converted back into acetyl CoA and used by the brain. Beta-hydroxybutyrate and acetoacetate spontaneously breakdown into acetone, which is excreted by the lungs, giving the breath a 'fruity' smell.
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    (Original post by Jpw1097)
    Insulin doesn't stimulate uptake of ketones. Insulin inhibits hormone-sensitive lipase (HSL) in adipocytes, therefore low levels of insulin lead to activation of HSL, causing free fatty acids to be released into the blood. These free fatty acids undergo beta-oxidation to form acetyl CoA which would normally enter the Krebs cycle/TCA cycle. However, as you've said, insulin inhibitis gluconeogenesis; therefore low levels of insulin stimulate gluconeogenesis, causing intermediates in the TCA cycle (such as oxaloacetate) to enter the gluconeogenic pathway to produce glucose. The depletion of these intermediates necessary for the TCA cycle inhibits the TCA cycle. Instead of the acetyl CoA entering the TCA cycle, it is converted to ketone bodies instead (beta-hydroxybutyrate, acetoacetate, and acetone), which can be converted back into acetyl CoA and used by the brain. Beta-hydroxybutyrate and acetoacetate spontaneously breakdown into acetone, which is excreted by the lungs, giving the breath a 'fruity' smell.
    Hi,
    Thank you for this comment - very impressive and detailed pathobiochemistry - out of interest, are you a biochemistry graduate or are you an endocrinologist? Apologies if I misled anyone, but my biochemistry knowledge is only as a medical student, and possibly slightly dated!
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    (Original post by macpatelgh)
    Hi,
    Thank you for this comment - very impressive and detailed pathobiochemistry - out of interest, are you a biochemistry graduate or are you an endocrinologist? Apologies if I misled anyone, but my biochemistry knowledge is only as a medical student, and possibly slightly dated!
    Just a second year medical student.
 
 
 
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