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Physiology Metabolism > Metabolism 5: Glycogen > Flashcards

Metabolism 5: Glycogen Flashcards

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?

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?

A

Activate PKA or inhibit phosphoprotein phosphatase to promote glycogen degradation

25
Q

How does insulin regulate glycogen synthesis/degradation?

A

Inhibits glycogen phosphorylase by stimulating phosphoprotein phosphatase which dephosphorylates the glycogen phosphorylase, inactivating it

26
Q

Which hormone promotes glycogen storage/degradation?

A

Storage: insulin
Degradation: glucagon

27
Q

When would you have high levels of AMP?

A

During exercise

28
Q

How does AMP regulate glycogen levels?

A

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
Q

What happens to glycogen levels when glucose and ATP are high?

A

Glucose and ATP bind directly to the active form of glycogen phosphorylase to inactivate its activity

30
Q

What activates glycogen synthase?

A

Dephosphorylation; Leads to glycogen synthesis

Phosphorylation inactivates glycogen synthase and thus inhibits glycogen sythesis

31
Q

What does insulin promote with regards to glycogen synthase?

A

Insulin activates phosphoprotein phosphatase to dephosphorylate glycogen synthase -> promotes glycogen synthesis

32
Q

What do the secondary messengers cAMP, Ca2+ and DAG do on glycogen synthase?

A

Activates phosphoryl kinase, calmodulin depdendent protein kinase, and PKC to promote phosphorylation of glycogen synthase -> inhibits glycogen synthesis

33
Q

What happens to glycogen synthase when G6Plevels are high?

A

G6P can bind to the inactivated (phosphorylated) form of glycogen synthase and allosterically activate it to promote glycogen synthesis (seen in GSDs)

34
Q

What is the overall effect of increased cAMP in liver?

A

Promote glycogen degradation
Inhibit glycolysis
Inhibit glycogen synthesis

35
Q

What is the overall effect of increased cAMP in heart and skeletal muscle

A

Promote glycogen degradation
Activate glycolysis
Inhibit glycogen syntehsis

36
Q

How does the phosphoinositide mechanism proceed?

A

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
Q

How does insulin affect glycogen levels

A

Insulin promotes glycogen synthesis in both the muscle and liver

38
Q

What is the sequence for forming and degrading glycogen?

A

synthesis: Glucose ->G6P ->G1P ->UDP-glucose -> glycogen

Degradation: Glcyogen -> G1P -> G6P -> glucose

39
Q

What can inherited glycogen storage disease affect?

A

Tissue levels of glycogen
Fasting blood glucose levels
lipid metabolism

40
Q

GSDs: Type 1 Von Gierke’s Disease

A

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
Q

GSDs: Type II Pompe’s Disease

A

Defective 1,4-glucosidase
Organs: all
Glycogen: Massive increase in normal structure
Clinical: Cardiorespiratory failure, Death usually before 2yo

42
Q

GSDs: Type III Cori’s Disease

A

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
Q

GSDs: Type IV Anderson’s Disease

A

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
Q

GSDs: Type V McArdle’s Disease

A

Defective Phosphorylase
Organs: Muscle
Glycogen: Moderate amount of normal structure
Clinical: Can’t perform strenuous exercise, painful muscle cramps

45
Q

GSDs: Type VI Hers’ Disease

A

Defective phosphorylase
Organ: Liver
Glycogen: Increased amount
Clinical: Like Von Gierke’s but milder

46
Q

GSDs: Type VII

A

Defective PFK-1
Organ: Muscle
Glycogen: Increased
clinical: Like Type V McArdle’s

47
Q

GSDs: Type VIII

A

Defective Phosphorylase Kinase
Organ: Liver
Glycogen: Increased normal
Clinical: Mild hepatomegaly, mild hypoglycemia

48
Q

What effects do glucagon and epinephrine have on glucose homeostasis

A 
Raise blood glucose
Promote hepatic gluconeogenesis
Promote hepatic glycogen degradation
Inhibit hepatic glycolysis
Inhibit hepatic glycogen synthesis
Block hepatic use of glucose
49
Q

How does glucagon/epi block hepatic glycolysis?

A

Inhibit PFK-2 -> dec F26bisphophate -> inhib PFK-1

Inhibit pyruvate kinase

50
Q

How does glucagon/epi promote hepatic gluconeogenesis?

A

Inhibit PFK-2 -> dec F26 bisphosphate -> promote F16phosphatase

Inhibit Pyruvate kinase

51
Q

What does the Pentose Phosphate Pathway do?

A

Generate NADPH for lipid biosynthesis
Generate Ribose-5-phosphate for biosynthesis of purine (DNA, RNA, etc)
Intermediates for glycolysis

52
Q

What is the rate limiting enzyme in the pentose phosphate pathway

A

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
Q

What are some glycolytic intermediates produced by the pentose phosphate pathway

A

glyceraldehyde 3 phosphate, F6P

54
Q

How much of glucose is used for the pentose phosphate pathway?

A

Only a small portion is diverted in this way

55
Q

What can lead to drug induced hemolytic anemia

A

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
Q

What is necessary to maintain glutathione in its reduced state? Why is this necessary?

A

NADPH. REduced GSH (glutathione) necessary to detoxify hydrogen peroxide (H2O2) and other reactive oxygen species

57
Q

What happens when NADPH levels are low in RBC?

A

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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