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생화학 14, 15장

생화학 14, 15장
25問 • 2年前
  • 김소영
    • 通報

    問題一覧

  • 1

    One consequence of starvation is a reduction in muscle mass. What happens to the muscle?

    The proteins degrade into amino acids, which can serve as substrates for gluconeogenesis.

  • 2

    What is the cost (in ATP equivalents) of transforming glucose to pyruvate via glycolysis and back again to glucose via gluconeogenesis? ATP equivalents per glucose molecule:

    4

  • 3

    Homeostatic mechanisms maintain the concentration of glucose in human blood plasma at about 5 mM. The concentration of free glucose inside a myocyte is much lower. Why is the concentration so low in the cell?

    Enzymes inside the cell convert glucose to other molecules.

  • 4

    What happens to glucose after entry into the cell?

    Hexokinase phosphorylates glucose to glucose 6-phosphate.

  • 5

    Physicians administer glucose intravenously as a food source in certain clinical situations. Given that the transformation of glucose to glucose 6-phosphate consumes ATP, why not administer intravenous glucose 6-phosphate instead?

    Glucose 6-phosphate cannot enter cells via glucose transporters or by diffusion.

  • 6

    Adults engaged in strenuous physical activity require an intake of about 160 g of carbohydrate daily but only about 20 mg of niacin for optimal nutrition. Given the role of niacin in glycolysis, how do you explain the observation?

    Synthesis of NAD+ utilizes dietary niacin, but one molecule of NAD+ can oxidize many thousands of glucose molecules.

  • 7

    Would shortening the glycolytic pathway in this way benefit the cell? Why or why not?

    No. Net production of ATP would be zero and growth could not occur under anaerobic conditions.

  • 8

    For a given concentration of fructose 6-phosphate, the PFK-1 activity increases with increasing concentrations of ATP, but there is a point beyond which increasing the concentration of ATP inhibits the enzyme. How does ATP regulate the activity of PFK-1?

    ATP binds to the catalytic site as a substrate, increasing PFK-1 activity., ATP binds to the allosteric site as an inhibitor, decreasing PFK-1 activity.

  • 9

    How do ATP levels regulate glycolysis?

    High levels of ATP inhibit glycolysis.

  • 10

    The inhibition of PFK-1 by ATP diminishes when the ADP concentration is high, as shown in the graph. What explains this observation?

    The [ATP]/[ADP] ratio regulates PFK-1 activity.

  • 11

    The clinical symptoms of two forms of galactosemia-galactokinase-deficiency galactosemia and transferase deficiency galactosemia show radically different severity. Although both types produce gastric discomfort after milk ingestion, deficiency of the transferase also leads to liver, kidney, spleen, and brain dysfunction and eventual death. What product accumulates in the blood and tissues with galactokinase-deficiency galactosemia?

    galactose

  • 12

    What product accumulates in the blood and tissues with transferase-deficiency galactosemia?

    galactose-1-phosphate

  • 13

    The clinical symptoms of two forms of galactosemia-galactokinase-deficiency galactosemia and transferase deficiency galactosemia show radically different severity. Although both types produce gastric discomfort after milk ingestion, deficiency of the transferase also leads to liver, kidney, spleen, and brain dysfunction and eventual death. What can you conclude about the relative toxicities of these products?

    Galactose 1-phosphate is more toxic that galactose

  • 14

    identify the carbon atom in pyruvate that would be labeled

    A

  • 15

    Suppose a researcher introduces a mutation into the glucosidase domain of the mammalian glycogen debranching enzyme. The mutation inhibits the activity of the glucosidase but does not affect the other functions of the enzyme. The researcher then introduces the mutated enzyme into mammalian cells that do not express wild type glycogen debranching enzyme. Predict the effect of the mutation on glycogen metabolism.

    glycogen molecules with branches containing a single glucose residue

  • 16

    Predict which product of the phosphoglucomutase reaction predominates when insulin levels are high.

    glucose 1-phosphate

  • 17

    How do the levels of AMP, ATP, citrate, and acetyl-CoA affect the flow of metabolites through glycolysis?

    ATP inhibits glycogen phosphorylase and PFK-1., AMP stimulates glycogen phosphorylase and PFK-1., Acetyl-CoA inhibits pyruvate kinase., Citrate inhibits PFK-1.

  • 18

    The Vmax of the glycogen phosphorylase from skeletal muscle is much greater than the Vmax of the same enzyme from liver tissue. What is the physiological function of glycogen phosphorylase in skeletal muscle?

    Glycogen breakdown supplies energy via ATP from glycolysis.

  • 19

    The Vmax of the glycogen phosphorylase from skeletal muscle is much greater than the Vmax of the same enzyme from liver tissue. What is the physiological function of glycogen phosphorylase in liver tissue?

    Glycogen breakdown maintains a steady level of blood glucose between meals.

  • 20

    Why does the Vmax of the muscle enzyme need to be greater than that of the liver enzyme?

    Actively working muscle must be able to produce ATP very quickly from glycogen breakdown.

  • 21

    What are the effects on glycogen metabolism when protein kinase A (PKA) loses the cAMP-binding site from its regulatory subunit? 답 2개

    Glucagon and epinephrine are unable to activate glycogen phosphorylase., Gluconeogenesis stimulation does not occur when blood glucose is low, leading to dangerously low blood glucose during periods of fasting.

  • 22

    What is the effect on glycogen metabolism when the protein phosphatase (PP1) inhibitor fails to function?

    PP1 continues to activate glycogen synthase and inhibit glycogen phosphorylase through dephosphorylation.

  • 23

    What is the effect on glycogen metabolism when the liver overexpresses phosphorylase b kinase?

    Phosphorylase remains phosphorylated and active, increasing the breakdown of glycogen.

  • 24

    What is the effect on glycogen metabolism when the liver expresses defective glucagon receptors?

    Low blood glucose levels do not stimulate gluconeogenesis, leading to a dangerous degree of hypoglycemia when fasting.

  • 25

    Which statements describe the hormone-stimulated process that triggers glucose production by the liver? 답 4개

    Epinephrine stimulates an enzyme cascade involving hepatic protein kinase A (PKA) and phosphorylase b kinase, which eventually leads to glycogen breakdown in the liver., The decrease in [fructose 2,6-bisphosphate] stimulates FBPase-1, the key enzyme in gluconeogenesis., Glucagon stimulates cAMP-dependent phosphorylation of PFK-2/FBPase-2, which decreases [fructose 2,6-bisphosphate)., The rapid decrease in blood glucose levels triggers glucagon release by the pancreas.

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    問題一覧

  • 1

    One consequence of starvation is a reduction in muscle mass. What happens to the muscle?

    The proteins degrade into amino acids, which can serve as substrates for gluconeogenesis.

  • 2

    What is the cost (in ATP equivalents) of transforming glucose to pyruvate via glycolysis and back again to glucose via gluconeogenesis? ATP equivalents per glucose molecule:

    4

  • 3

    Homeostatic mechanisms maintain the concentration of glucose in human blood plasma at about 5 mM. The concentration of free glucose inside a myocyte is much lower. Why is the concentration so low in the cell?

    Enzymes inside the cell convert glucose to other molecules.

  • 4

    What happens to glucose after entry into the cell?

    Hexokinase phosphorylates glucose to glucose 6-phosphate.

  • 5

    Physicians administer glucose intravenously as a food source in certain clinical situations. Given that the transformation of glucose to glucose 6-phosphate consumes ATP, why not administer intravenous glucose 6-phosphate instead?

    Glucose 6-phosphate cannot enter cells via glucose transporters or by diffusion.

  • 6

    Adults engaged in strenuous physical activity require an intake of about 160 g of carbohydrate daily but only about 20 mg of niacin for optimal nutrition. Given the role of niacin in glycolysis, how do you explain the observation?

    Synthesis of NAD+ utilizes dietary niacin, but one molecule of NAD+ can oxidize many thousands of glucose molecules.

  • 7

    Would shortening the glycolytic pathway in this way benefit the cell? Why or why not?

    No. Net production of ATP would be zero and growth could not occur under anaerobic conditions.

  • 8

    For a given concentration of fructose 6-phosphate, the PFK-1 activity increases with increasing concentrations of ATP, but there is a point beyond which increasing the concentration of ATP inhibits the enzyme. How does ATP regulate the activity of PFK-1?

    ATP binds to the catalytic site as a substrate, increasing PFK-1 activity., ATP binds to the allosteric site as an inhibitor, decreasing PFK-1 activity.

  • 9

    How do ATP levels regulate glycolysis?

    High levels of ATP inhibit glycolysis.

  • 10

    The inhibition of PFK-1 by ATP diminishes when the ADP concentration is high, as shown in the graph. What explains this observation?

    The [ATP]/[ADP] ratio regulates PFK-1 activity.

  • 11

    The clinical symptoms of two forms of galactosemia-galactokinase-deficiency galactosemia and transferase deficiency galactosemia show radically different severity. Although both types produce gastric discomfort after milk ingestion, deficiency of the transferase also leads to liver, kidney, spleen, and brain dysfunction and eventual death. What product accumulates in the blood and tissues with galactokinase-deficiency galactosemia?

    galactose

  • 12

    What product accumulates in the blood and tissues with transferase-deficiency galactosemia?

    galactose-1-phosphate

  • 13

    The clinical symptoms of two forms of galactosemia-galactokinase-deficiency galactosemia and transferase deficiency galactosemia show radically different severity. Although both types produce gastric discomfort after milk ingestion, deficiency of the transferase also leads to liver, kidney, spleen, and brain dysfunction and eventual death. What can you conclude about the relative toxicities of these products?

    Galactose 1-phosphate is more toxic that galactose

  • 14

    identify the carbon atom in pyruvate that would be labeled

    A

  • 15

    Suppose a researcher introduces a mutation into the glucosidase domain of the mammalian glycogen debranching enzyme. The mutation inhibits the activity of the glucosidase but does not affect the other functions of the enzyme. The researcher then introduces the mutated enzyme into mammalian cells that do not express wild type glycogen debranching enzyme. Predict the effect of the mutation on glycogen metabolism.

    glycogen molecules with branches containing a single glucose residue

  • 16

    Predict which product of the phosphoglucomutase reaction predominates when insulin levels are high.

    glucose 1-phosphate

  • 17

    How do the levels of AMP, ATP, citrate, and acetyl-CoA affect the flow of metabolites through glycolysis?

    ATP inhibits glycogen phosphorylase and PFK-1., AMP stimulates glycogen phosphorylase and PFK-1., Acetyl-CoA inhibits pyruvate kinase., Citrate inhibits PFK-1.

  • 18

    The Vmax of the glycogen phosphorylase from skeletal muscle is much greater than the Vmax of the same enzyme from liver tissue. What is the physiological function of glycogen phosphorylase in skeletal muscle?

    Glycogen breakdown supplies energy via ATP from glycolysis.

  • 19

    The Vmax of the glycogen phosphorylase from skeletal muscle is much greater than the Vmax of the same enzyme from liver tissue. What is the physiological function of glycogen phosphorylase in liver tissue?

    Glycogen breakdown maintains a steady level of blood glucose between meals.

  • 20

    Why does the Vmax of the muscle enzyme need to be greater than that of the liver enzyme?

    Actively working muscle must be able to produce ATP very quickly from glycogen breakdown.

  • 21

    What are the effects on glycogen metabolism when protein kinase A (PKA) loses the cAMP-binding site from its regulatory subunit? 답 2개

    Glucagon and epinephrine are unable to activate glycogen phosphorylase., Gluconeogenesis stimulation does not occur when blood glucose is low, leading to dangerously low blood glucose during periods of fasting.

  • 22

    What is the effect on glycogen metabolism when the protein phosphatase (PP1) inhibitor fails to function?

    PP1 continues to activate glycogen synthase and inhibit glycogen phosphorylase through dephosphorylation.

  • 23

    What is the effect on glycogen metabolism when the liver overexpresses phosphorylase b kinase?

    Phosphorylase remains phosphorylated and active, increasing the breakdown of glycogen.

  • 24

    What is the effect on glycogen metabolism when the liver expresses defective glucagon receptors?

    Low blood glucose levels do not stimulate gluconeogenesis, leading to a dangerous degree of hypoglycemia when fasting.

  • 25

    Which statements describe the hormone-stimulated process that triggers glucose production by the liver? 답 4개

    Epinephrine stimulates an enzyme cascade involving hepatic protein kinase A (PKA) and phosphorylase b kinase, which eventually leads to glycogen breakdown in the liver., The decrease in [fructose 2,6-bisphosphate] stimulates FBPase-1, the key enzyme in gluconeogenesis., Glucagon stimulates cAMP-dependent phosphorylation of PFK-2/FBPase-2, which decreases [fructose 2,6-bisphosphate)., The rapid decrease in blood glucose levels triggers glucagon release by the pancreas.