1. Describe the glycogen molecule.
- Glycogen is the storage form of glucose
-it is a large branched polysaccharide with a molecular weight between 10-100 million
- it is made from glucosyl units linked by alpha 1-4 glycosidic and alpha 1-6 glycosidic bonds that occur every 8-10 residues
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2. What are the functions of glycogen in liver and skeletal muscle? Why must glucose-6-phosphate produced from glycogen in muscle enter glycolysis? Why does glucose produced from glycogen in liver usually enter the blood stream instead of glycolysis?
-Glycogen in liver: to provide glucose for the blood
-Glycogen in muscle: to provide glucose for energy production for muscle contraction
- Glucose-6-phosphate produced from glycogen must enter glycolysis because it does not have Glucose 6-phosphatase lik
3. What effect does glucagon have upon glycogenolysis and gluconeogenesis in the liver?
It has a positive effect and activates those pathways.
4. Use the activation or inhibition of glycogen synthesis or glycogenolysis to explain the concept of a futile cycle and how a futile cycle is usually prevented. (28.3)
Futile cycle: a cycle where substrate -> product in one pathway is then converted back from product-> substrate in another pathway - it wastes the energy of the phosphate bonds
- prevention: using different pathways that involve different control enzymes.
5. Describe the pathway for glycogen synthesis from glucose in liver and muscle: Name, Function, Substrates, Products, Control Enzyme, Regulation, Compartment. (28.3)
Name: Glycogen Synthesis or Glycogenesis
Function:
Liver: Stores glucose so you can maintain blood glucose at a later time
Muscle: Stores glucose so you can use it for energy contractions at a later time
Substrates: ATP,glucose, UTP
Products: ADP,UDP, pyr
6. Describe the pathway for glycogen degradation to glucose or glucose-6-phosphate in liver and muscle: Name, Function, Substrates, Products, Control Enzyme, Regulation, Compartment. (28.3)
Name: Glycogenolysis, glycogen degradation, phosphoryolysis
Function: Provide blood glucose (liver). Provide glucose to produce energy for muscle contrations (muscle)
Substrates: Glycogen, inorganic phosphate (P)
Products: Glucose-6-P and Glucose
Control
7. Briefly, what is Von Gierke's disease? What is McArdle's disease?
Von Gierke's Disease: deficiency of Glucose-6-phosphatase in the liver. Means the liver can't release free glucose into the blood. Both gluconeogenesis and gluconeogenesis are inhibited
McArdle's disease: it is a lack of glycogen phosphorylase in muscle.
8. What is the effect of a high carbohydrate meal, fasting, or stress upon the blood concentrations of insulin, glucagon, and epinephrine?
High carbohydrate meal: increased insulin, decreased glucagon, decreased epinephrine (and cortisol)
Fasting: Decreased insulin, increased glucagon, epinephrine and cortisol rise slowly
Stress: insulin decreases and stress hormones go up
9. What is the effect of a high carbohydrate meal upon blood glucose and the glucose in liver cells?
blood glucose: immediately increase and result in increased insulin
Glucose in liver cells: blood glucose and insulin will activate glycogen synthesis in liver and insulin will inhibit glycogenolysis
Insulin will activate glycolysis and inhibit gluconeoge
10. What is the effect of changes in the insulin/glucagon ratio, blood glucose or epinephrine upon glycogen synthesis and glycogen degradation in the liver?
Glycogen Synthesis in the liver: activated by increased insulin/glucagon ratio, increased glucose in the blood, and the decrease in level of epinephrine
Glycogen Degradation in the liver: activated by the decreased insulin/glucagon ratio, by a decrease in
11. What is the effect of changes in the insulin, blood glucose or epinephrine upon glycogen synthesis or glycogen degradation in muscle? Error in fourth edition, Table 28.2: Exercise does not decrease either AMP or glycogen degradation in muscle cells.
Glycogen synthesis: increases with the rise of insulin, decreases as it goes down. Rising blood glucose increases synthesis and decreasing levels inhibit synthesis.
Glycogen degredation: increases with a decrease in insulin, with the release of epinephrin
12. In order of their activation, be able to name and give the reason for the activation of all the intermediates in the cAMP cascade in liver. Start with a decrease in the insulin/glucagon ratio or an increase in epinephrine and end with the change in ac
- glucagon or epinephrine binds to their respective cell membrane receptors and change the receptor conformation
- the receptor with its new conformation binds to Gs (G stimulatory protein) and changes its conformation sot that it can exchange GDT for GTP
13. What role does protein phosphatase have in the cAMP cascade? How is protein phosphatase activated or inhibited?
Protein phosphatase (activated by insulin, inhibited by epinephrine and glucagon, and the cAMP cascade)
-stops the cAMP cascade when it removes the phosphates from phosphorylase kinase and glycogen synthase .
- it activates Glycogen synthase by removing i
14. What is the effect of insulin upon the cAMP cascade?
Insulin inhibits the cAMP cascade:
1. it activates cAMP phosphodiesterase which converts cAMP to AMP inhibiting the activation of protein kinase A
2. Insulin activates protein phosphatase
3. insulin inhibits the secretion of glucagon by alpha-cells of the
15. Following the ingestion of carbohydrate, the glucose concentration in the cytosol of liver cells increases. What effect does this have upon phosphorylase a?
Glucose inhibits liver glycogen phophorylase a by dephosphorylating it. This way glucose has a direct and immediate inhibitory effect on glycogen degradation, even before insulin levels rise
16. When the insulin to glucagon ratio is low as it usually is in both Type I and Type II diabetics, how is the storage of glucose in muscle and liver affected after a high carbohydrate meal? Why? What happens to blood glucose?
The storage of glucagon is inhibited because the lower level of insulin in the blood is not stimulating glucose uptake appropriately. In the muscle cells the slower uptake is because of a lower than normal Glut-4 presence, and in the liver because the pat
17. In order of their activation, be able to name and give the reason for the activation of the intermediates in the inositol trisphosphate and diacylglycerol cascade in liver. Start with epinephrine binding to an a1-receptor and finish with the change in
- Epinephrine binds to an alpha-1 adrenergic receptor on the cell membrane - receptor changes shape
-altered receptor then binds to a Gq-protein and it changes conformation
- resulting in GDP being exchanged for GTP and the trimeric protein dissociating t
18. What are the three major activators of phosphorylase in muscle?
1. AMP from muscle contraction serves as an allosteric activator of glycogen phosphorylase b, the active form is glycogen phosphorylase a (which catalyzes glycogenolysis).
2. Ca2+ from the muscle contraction (in liver is from a1-receptor activation and it
19. Concerning Getta Carbo: Compare the relative concentrations of insulin, glucagon, and epinephrine before labor and after delivery. Why was her blood glucose low? Why is the oxidation of fatty acids by the liver important during the first five or six h
Before birth: an infant would normally have constant glucose and therefore constant and high insulin, leading to glycogen store buildup.
after Birth: blood glucose would decrease after the umbilical cord was cut. This with the stress of birth would lead t
20. Concerning Jim Bodie: Jim injected insulin just before exercise. What were the affects upon the pathways and transport mechanisms of the liver and muscle that led to his hypoglycemic coma?
-Insulin inactivated glycogenolysis in skeletal muscle and the liver, along with gluconeogenesis. His blood glucose was quickly used up as it was also being synthesized into glycogen, and he was in trouble!!