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Physiology Metabolism > Metabolism 5: Glycogen > Flashcards

Metabolism 5: Glycogen Flashcards

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1
Q

What is glycogen composed of?

A

Glycosyl residues mostly of a-1,4 glycosidic linkages and branching a-1.6 glycosidic linkages

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2
Q

What happens to hepatic glycogen concetration as meal time varies?

A

Increases after meals

Decreases in between meals

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3
Q

What’s the difference between muscle glycogen and liver glycogen interms of function

A

Muscle glycogen is fuel reserve for ATP production within that muscle

Liver glycogen serves as a reserve for maintainig blood glucose

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4
Q

What’s the limit that liver can store for glycogen? What happens to excess glucose?

A

100 g of glycogen

Excess glucose is redirected to fatty acid synthesis

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5
Q

What does glycogen synthase do?

A

key enzyme that adds glucose-1-phosphate to growing glycogen chains

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6
Q

What does glycogen phosphorylase do?

A

remove glucose moieties from glycogen

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7
Q

Why can liver contribute its glucose from glycogen directly to blood?

A

Liver has glucose 6 phosphatase that converts G6P to glucose and allows it to exit the liver and enter circulation

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8
Q

Why can’t the muscle glycogen contribute to blood glucose levels?

A

muscle does not express glucose 6 phosphatase, so G6P cannot leave the cell and is thus used for ATP production

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9
Q

How much glycogen can muscle store and what happens to excess glucose?

A

400 g of glycogen

Excess converted to FAs and stored as TGs

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10
Q

When is muscle glycogen mobilized?

A

During exercise

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11
Q

What is the sequence of events after a meal for hepatic glycogen synthesis?

A

Glucose from blood enters liver via GLUT2 -> converted to G6P -> Insulin stimulate glycogen formation, fatty acid biosynthesis , or glycolysis to use as fuel

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12
Q

What is the sequence of events during a fast for hepatic glycogen

A

Glucagon released by pancreas -> stimulates liver to undergo glycogenolysis -> release G6P -> glucose-6-phosphatase converts it to glucose -> glucose leaves liver via GLUT-2 into blood

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13
Q

What is the sequence of events for muscle glycogen after a meal?

A

Insulin stimulates glucose uptake by muscle via GLUT4 from blood -> converts to G6P -> forms glycogen or undergoes glycolysis and CAC

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14
Q

What is the sequence of events for muscle glycogen during exercise?

A

Epinephrine stimulates glycogenolysis via beta receptors -> convert glucose to G6P -> use in glycolysis and CAC for energy

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15
Q

What energy source is used during exercise at the beginning?

A

ATP + Creatine phosphate —> Anaerobic Glycolysis (Muscle Glycogen)

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16
Q

What energy source is used in prolonged exercise?

A

Aerobic Oxidation
Muscle glycogen, plasma glucose, liver glycogen

Much later, start using plasma FFA and adipose tissue triglycerides

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17
Q

What enzymes are required for glycogen synthesis?

A

Glycogen synthase: adds glucosyl units in a-1,4 links

Branching enzyme: adds glucosyl units in a-1,6 links

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18
Q

What enzymes are required for glycogen degradation?

A

Glycogen Phosphorylase: removes glucosyl units from a-1,4-links
Debranching Enzyme: transferase activity and removes a-1,6 links (glucosidase activity)
Kinases to activate Glycogen Phosphorylase

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19
Q

What is Glycogenin?

A

Polypeptide primer used for glycogen synthesis

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20
Q

Osmotically, what’s the difference between glucose and glycogen?

A

Glycogen is not osmotically active while glucose is

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21
Q

Why are secondary messenger systems pertinent for glycogen equilibrium?

A

Can activate glycogen degradation or inhibit glycogen syntehsis by activating or inhibiting glycogen phosphorylase and glycogen synthase, respectively

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22
Q

What are some of the secondary messengers regulating glycogen formation/degradation?

A

cAMP ->PKA -> activate phosphorylkinase
PI -> DAG and IP3 -> Ca2+ -> activate Phosphorylkinase
Ca2+ -> activate phosphoryl kinase

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23
Q

What does activating phosphoryl kinase do?

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A

Phosphorylates glycogen phosphorylase to convert it from its inactive b form to active a form

Promotes glycogen degradation

24
Q

What does cAMP do for glycogen equilibrium?

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A

Activate PKA or inhibit phosphoprotein phosphatase to promote glycogen degradation

25
How does insulin regulate glycogen synthesis/degradation?
Inhibits glycogen phosphorylase by stimulating phosphoprotein phosphatase which dephosphorylates the glycogen phosphorylase, inactivating it
26
Which hormone promotes glycogen storage/degradation?
Storage: insulin Degradation: glucagon
27
When would you have high levels of AMP?
During exercise
28
How does AMP regulate glycogen levels?
Directly binds to the b form of glycogen phosphorylase to activate it regardless of phosphorylation status Overrides inhibitory effect of ATP Promotes glycogen degradation
29
What happens to glycogen levels when glucose and ATP are high?
Glucose and ATP bind directly to the active form of glycogen phosphorylase to inactivate its activity
30
What activates glycogen synthase?
Dephosphorylation; Leads to glycogen synthesis | Phosphorylation inactivates glycogen synthase and thus inhibits glycogen sythesis
31
What does insulin promote with regards to glycogen synthase?
Insulin activates phosphoprotein phosphatase to dephosphorylate glycogen synthase -> promotes glycogen synthesis
32
What do the secondary messengers cAMP, Ca2+ and DAG do on glycogen synthase?
Activates phosphoryl kinase, calmodulin depdendent protein kinase, and PKC to promote phosphorylation of glycogen synthase -> inhibits glycogen synthesis
33
What happens to glycogen synthase when G6Plevels are high?
G6P can bind to the inactivated (phosphorylated) form of glycogen synthase and allosterically activate it to promote glycogen synthesis (seen in GSDs)
34
What is the overall effect of increased cAMP in liver?
Promote glycogen degradation Inhibit glycolysis Inhibit glycogen synthesis
35
What is the overall effect of increased cAMP in heart and skeletal muscle
Promote glycogen degradation Activate glycolysis Inhibit glycogen syntehsis
36
How does the phosphoinositide mechanism proceed?
Epi binds to a-adrenergic receptor -> PIP2 cut by PLC -> IP3 and DAG released -> IP3 binds to ER to promote Ca2+ release and DAG activates PKC -> Ca2+ activates Ca2+ dependent PK -> stimulate glycogenolysis
37
How does insulin affect glycogen levels
Insulin promotes glycogen synthesis in both the muscle and liver
38
What is the sequence for forming and degrading glycogen?
synthesis: Glucose ->G6P ->G1P ->UDP-glucose -> glycogen Degradation: Glcyogen -> G1P -> G6P -> glucose
39
What can inherited glycogen storage disease affect?
Tissue levels of glycogen Fasting blood glucose levels lipid metabolism
40
GSDs: Type 1 Von Gierke's Disease
Defective G6Phosphatase Organs: Liver and kidney Glycogen: increased normal structure Clinical: hepatomegaly, failure to thrive, hypoglycemia, increased lactate, hyperuricemia, hyperlipidemia, gouty arthritis, mental retardation, hyperlipidemia
41
GSDs: Type II Pompe's Disease
Defective 1,4-glucosidase Organs: all Glycogen: Massive increase in normal structure Clinical: Cardiorespiratory failure, Death usually before 2yo
42
GSDs: Type III Cori's Disease
Defective amylo-1,6 debranching enzyme Organs: Muscle and liver Glycogen: increased short outer Clinical: Similar to type 1 Von Gierke's but milder
43
GSDs: Type IV Anderson's Disease
Defective Branching Enzyme Organs: Liver and Spleen Glycogen: Normal amount with long branches Clinical: Cirrhosis of liver, liver death before 2 yo leads to death
44
GSDs: Type V McArdle's Disease
Defective Phosphorylase Organs: Muscle Glycogen: Moderate amount of normal structure Clinical: Can't perform strenuous exercise, painful muscle cramps
45
GSDs: Type VI Hers' Disease
Defective phosphorylase Organ: Liver Glycogen: Increased amount Clinical: Like Von Gierke's but milder
46
GSDs: Type VII
Defective PFK-1 Organ: Muscle Glycogen: Increased clinical: Like Type V McArdle's
47
GSDs: Type VIII
Defective Phosphorylase Kinase Organ: Liver Glycogen: Increased normal Clinical: Mild hepatomegaly, mild hypoglycemia
48
What effects do glucagon and epinephrine have on glucose homeostasis
``` Raise blood glucose Promote hepatic gluconeogenesis Promote hepatic glycogen degradation Inhibit hepatic glycolysis Inhibit hepatic glycogen synthesis Block hepatic use of glucose ```
49
How does glucagon/epi block hepatic glycolysis?
Inhibit PFK-2 -> dec F26bisphophate -> inhib PFK-1 Inhibit pyruvate kinase
50
How does glucagon/epi promote hepatic gluconeogenesis?
Inhibit PFK-2 -> dec F26 bisphosphate -> promote F16phosphatase Inhibit Pyruvate kinase
51
What does the Pentose Phosphate Pathway do?
Generate NADPH for lipid biosynthesis Generate Ribose-5-phosphate for biosynthesis of purine (DNA, RNA, etc) Intermediates for glycolysis
52
What is the rate limiting enzyme in the pentose phosphate pathway
Glucose-6-phosphate dehydrogenase Deficiency leads to hemolytic anemia due to inability of RBCs to maintain adequate levels of NADPH necessary to reduce glutathione that reduces SH on proteins
53
What are some glycolytic intermediates produced by the pentose phosphate pathway
glyceraldehyde 3 phosphate, F6P
54
How much of glucose is used for the pentose phosphate pathway?
Only a small portion is diverted in this way
55
What can lead to drug induced hemolytic anemia
Deficiency in G6PDH leads to hemolytic anemia due to inability of RBCs to maintain adequate levels of NADPH necessary to reduce glutathione that reduces SH on proteins and thus protect RBCs from oxidative damage
56
What is necessary to maintain glutathione in its reduced state? Why is this necessary?
NADPH. REduced GSH (glutathione) necessary to detoxify hydrogen peroxide (H2O2) and other reactive oxygen species
57
What happens when NADPH levels are low in RBC?
Decreased in reduced form of glutathione (GSH) and thus increased levels of hydrogen peroxide and levels of oxidative damage

Physiology Metabolism (11 decks)

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