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BQ II > T3. GLYCOGEN METABOLISM > Flashcards

T3. GLYCOGEN METABOLISM Flashcards

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1
Q

What is glycogen made of?

A

Glycogen is formed by D-glucose polysaccharide linked by O-glycosidic bonds: α-1,4 and α-1,6 (branches every 8–12 residues).

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2
Q

How many residues and what size does glycogen typically have?

A

Glycogen contains around 55,000 residues and measures 10–40 nm.

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3
Q

What are glycogen’s solubility and mobilization characteristics?

A

Glycogen has high solubility and allows for quick mobilization of glucose.

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4
Q

How many reducing and non-reducing ends does glycogen have?

A

Glycogen has one reducing end and multiple non-reducing ends—one per branch plus one.

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5
Q

Why are non-reducing ends in glycogen important?

A

Glycogen-degrading and synthesizing enzymes attach to non-reducing ends to release glucose.

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6
Q

How does glycogen avoid osmotic pressure problems?

A

The branching structure allows glucose storage without affecting osmotic pressure.

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7
Q

What advantage does glycogen’s structure offer in energy mobilization?

A

Multiple non-reducing ends allow very fast glucose release (quick mobilization).

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8
Q

Where is glycogen stored in the body?

A

Glycogen is stored in cytoplasmic granules—10% in the liver and 1–2% in muscles.

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9
Q

Why isn’t all energy stored as fat? (1/3)

A
  1. Fats cannot provide energy quickly; they have slow mobilization.
    2.Fats cannot be metabolized under anaerobic conditions, unlike glucose.
    3.Fatty acids are not precursors for glucose, so they can’t maintain glucose homeostasis.
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10
Q

What is the role of liver glycogen?

A

Liver glycogen maintains blood glucose levels by hydrolyzing G6P into glucose and releasing it into the bloodstream.

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11
Q

What enzyme allows the liver to release glucose into the blood?

A

Glucose 6-phosphatase (G6Pase), present in hepatocytes.

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12
Q

Why can’t muscles release glucose into the bloodstream?

A

Muscles lack G6Pase, so they cannot convert G6P into free glucose.

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13
Q

What is the role of muscle glycogen?

A

Muscle glycogen serves only as a fuel reserve for the muscle cell (ATP synthesis).

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14
Q

Characteristics of red muscle fibers

A

Aerobic, slow contraction, high blood supply, many mitochondria; use complete glucose oxidation.

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15
Q

Characteristics of white muscle fibers

A

Anaerobic, fast contraction, low blood supply, few mitochondria; rely heavily on glycolysis and need large glycogen stores.

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16
Q

What is glycogenesis?

A

The process of glycogen synthesis from glucose, involving five enzymatic steps.

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17
Q

Phosphoglucomutase reaction and role

A

Converts G6P to G1P reversibly; phosphate is transferred from serine to C1 and back to serine from C6.

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18
Q

Reaction catalyzed by G1P uridyltransferase

A

G1P + UTP → UDP-Glucose + 2Pi; activates glucose for synthesis.

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19
Q

Why is UDP-Glucose important in glycogenesis?

A

It makes glucose donation exergonic, overcoming the endergonic direct binding to glycogen.

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20
Q

Reaction catalyzed by glycogen synthase

A

Glycogen(n) + UDP-Glucose → Glycogen(n+1) + UDP; forms α(1–4) glycosidic bonds.

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21
Q

Requirements of glycogen synthase activity

A

Needs a pre-formed primer chain of at least 7–8 glucose residues.

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22
Q

Is glycogen synthase reaction reversible or regulatory?

A

It is an exergonic, regulatory step in glycogenesis.

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23
Q

What does glycogen synthase produce in different tissues?

A

Produces different isomers of glycogen for hepatic and muscle tissues.

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24
Q

Role of the branching enzyme in glycogenesis

A

Transfers a 7-residue chain to C6 OH of a glucose residue, creating α(1–6) bonds; occurs ≥4 residues from another branch.

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25
Role and mechanism of glycogenin
Initiates glycogen synthesis by attaching glucose from UDP-Glucose to Tyr194, forming a primer chain of 7 residues.
26
What happens after glycogenin initiates the glycogen chain?
Glycogen synthase and branching enzyme take over to elongate and branch the chain.
27
What is glycogenolysis?
Breakdown of glycogen into glucose 6-phosphate, occurring in three steps.
28
What happens to G6P after glycogenolysis in the liver?
G6P is converted into glucose by G6Pase and released into the bloodstream.
29
What happens to G6P after glycogenolysis in the muscle?
G6P is used directly in glycolysis for ATP synthesis; not released into the blood.
30
Glycogen phosphorylase reaction
Glycogen(n) + Pi → Glycogen(n–1) + G1P; cleaves α-1,4 bonds at non-reducing ends via phosphorolysis.
31
What cofactor does glycogen phosphorylase require?
Pyridoxal phosphate (source of phosphate group).
32
What happens at branch points during glycogenolysis?
Glycogen phosphorylase stops 4 residues before a branch; debranching enzyme continues the breakdown.
33
Is glycogen phosphorylase reaction exergonic or endergonic?
It is exergonic under physiological conditions.
34
What is the main function of the debranching enzyme?
The enzyme moves the ramification limit to a linear chain of glycogen, leaving a branch with only one glucose molecule.
35
What happens after the debranching enzyme moves the ramification limit?
It breaks a (1 → 6) bond between this glucose and the glycogen chain, releasing a glucose (not phosphorylated).
36
How much glucose is lost in this process?
Around 10% of the glucose residues are lost, because they are not phosphorylated and leave the cell.
37
What other enzyme does the debranching enzyme act combined with?
It acts combined with glycogen phosphorylase and participates in glycosyl transferase activity.
38
What is the reaction catalyzed by phosphoglucomutase?
The reaction is G6P → G1P.
39
How does phosphoglucomutase catalyze this reaction?
The reaction begins with the phosphorylation of the Ser residue, where the enzyme donates its phosphoryl group to G1P producing glucose 1,6BP.
40
What happens after glucose 1,6BP is formed?
The phosphoryl group of 1,6BP is transferred back to the enzyme reforming the phosphoenzyme and giving rise to G6P.
41
Why is regulation important for synthesis and degradation pathways?
Synthesis and degradation pathways require coordination and reciprocity, so they must be regulated.
42
Which enzymes are highly regulated by allosteric effectors, covalent modifications, and hormonal regulation?
The key enzymes are glycogen phosphorylase (GP) and glycogen synthase (GS).
43
How is glycogen phosphorylase regulated?
Phosphorylation of phosphorylase makes it active, favoring glycogen degradation.
44
What happens when glycogen synthase is phosphorylated?
Phosphorylation of synthase triggers its deactivation, favoring glycogen degradation.
45
Where are PP1, glycogen synthase, and phosphorylase bound?
They are bound to the non-reducing ends of the glycogen molecule, and all enzymes act over the non-reducing end.
46
What is pyridoxal phosphate and its role?
Pyridoxal phosphate is a prosthetic group that provides the Pi group needed for the reaction.
47
What is the structure of glycogen phosphorylase?
Glycogen phosphorylase is a dimer with an N-terminal domain binding to glycogen and a C-terminal domain where the prosthetic group binds.
48
How do allosteric effectors and phosphorylation affect glycogen phosphorylase?
They bind to the dimer where both monomers form, and the catalytic site can be more or less exposed, giving rise to T-state and R-state conformations.
49
What is the difference between T-state and R-state?
T-state is less accessible and cannot be phosphorylated, whereas R-state is more accessible and can be phosphorylated.
50
Which conformations are present in muscle cells?
In muscle, phosphorylase b in the T-conformation is predominant (inactive), but it can be phosphorylated to phosphorylase a (active) which converts quickly to R-conformation.
51
How do allosteric effectors regulate phosphorylase activity in muscle?
When ATP is low, AMP binds to the T-state shifting the equilibrium towards R-state, improving glycogen degradation.
52
What happens when [ATP] and [G6P] are high in muscle?
High [ATP] and [G6P] trigger the T-state conformation, inhibiting glycogen degradation.
53
How is glycogen phosphorylase regulated in the liver?
When blood glucose levels increase, glucose binds to phosphorylase-a, shifting the equilibrium to T-state (inactive). Phosphorylase-a can also be phosphorylated to convert to phosphorylase-b.
54
How is phosphorylase kinase activated?
Phosphorylase kinase is activated by protein kinase A (PKA), which phosphorylates the α and β subunits.
55
What are the two ways to activate phosphorylase kinase?
Glucagon and adrenaline stimulate PKA production to phosphorylate α and β subunits, and muscle contraction releases Ca2+, binding to the δ subunit.
56
How do glucagon and adrenaline activate phosphorylase kinase?
They stimulate PKA to phosphorylate the α and β subunits, making PK partially active.
57
What happens during muscle contraction?
Muscle contraction releases Ca2+, which binds to the δ subunit, making PK partially active.
58
What hormones activate glycogen phosphorylase?
Glucagon (liver), Adrenaline (β receptors – liver, muscle), Nerve impulse (muscle), and Adrenaline (α - liver).
59
What hormone inhibits glycogen phosphorylase?
Insulin.
60
What happens when glycogen synthase is phosphorylated?
When phosphorylated, glycogen synthase is inactivated.
61
What activates glycogen synthase?
The enzyme is activated by G6P binding to glycogen synthase b, which exposes phosphorylation sites for PP1 to dephosphorylate it.
62
What role does PP1 play in glycogen metabolism?
PP1 dephosphorylates glycogen phosphorylase and glycogen synthase, regulating glycogen synthesis and degradation.
63
How is PP1 activity inhibited during glycogen degradation?
PKA activates glycogen phosphorylase to dephosphorylate PP1, inhibiting its activity and slowing down glycogen degradation.
64
How is PP1 activated during glycogen synthesis?
Insulin activates PP1, which binds to glycogen, increasing its activity and triggering glycogen synthesis.
65
What role does the liver play in glucose homeostasis?
It maintains blood glucose levels using glycogen phosphorylase as a glucose sensor.
66
What happens in the liver when blood glucose is low?
Glucagon is released and adrenaline increases
67
What is the effect of glucagon and β-adrenergic stimulation on the liver?
They increase intracellular cAMP and activate PKA
68
How does PKA influence glycogen metabolism in the liver?
It phosphorylates glycogen phosphorylase (activating) and glycogen synthase (inactivating).
69
What is the outcome of cAMP and PKA activity on glycolysis in the liver?
Glycolysis is inhibited
70
How is glucose released into the blood from the liver during hypoglycemia?
G6P is dephosphorylated by glucose-6-phosphatase and exported as glucose.
71
How does adrenaline interact with α-adrenergic receptors in the liver?
It activates phospholipase C
72
What is the function of DAG in liver glycogen metabolism?
DAG activates protein kinase C
73
What is the function of IP3 in liver glycogen metabolism?
IP3 promotes calcium release from the ER to cytosol.
74
How does cytosolic calcium affect glycogen metabolism in the liver?
It activates kinases that phosphorylate glycogen phosphorylase and synthase
75
What is the effect of high blood glucose levels on liver metabolism?
Insulin is released
76
What effect does PP1 have on glycogen enzymes in the liver?
PP1 dephosphorylates glycogen phosphorylase (inactivating it) and glycogen synthase (activating it).
77
How does insulin influence glycogen metabolism in the liver?
It inhibits degradation and stimulates glycogen synthesis to store excess glucose.
78
What is the primary function of glucose in muscle tissue?
It is used for the muscle's own energy needs.
79
What controls glycogen metabolism in muscle tissue?
Stress (adrenaline) and nerve impulses (acetylcholine).
80
What does adrenaline do in muscle tissue?
It increases cAMP and PKA activity
81
How does cAMP affect glycolysis in muscle?
It stimulates glycolysis
82
How is glycogen degradation linked to muscle contraction?
Calcium released from the ER triggers both contraction and glycogen breakdown.
83
What is insulin's effect on muscle glycogen metabolism?
It decreases cAMP
84
What additional action does insulin have in muscle?
It promotes glucose uptake via GLUT4.
85
What is the overall effect of insulin in both liver and muscle?
It inhibits glycogen breakdown and promotes glycogen synthesis.
86
What causes McArdle disease?
A deficiency of muscle glycogen phosphorylase.
87
What are the symptoms of McArdle disease?
Muscle pain and rapid fatigue during exercise
88
How does McArdle disease affect energy metabolism in muscle?
Leads to reliance on protein degradation and amino acid catabolism.
89
What causes Von Gierke disease?
A deficiency in glucose-6-phosphatase.
90
What organs are affected in Von Gierke disease?
Liver and kidneys accumulate excess glycogen.
91
What are the metabolic consequences of Von Gierke disease?
Severe hypoglycemia
92
Why does Von Gierke disease cause hyperlipidemia?
Excess glucose is converted to lactate

BQ II (17 decks)

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