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Protein Control in Cellular Regulation > Glycogen and Lipid Metabolism > Flashcards

Glycogen and Lipid Metabolism Flashcards

1
Q

What is glycogen?

A

A storage polysaccharide that is made up of glucose units.

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2
Q

What links long chains of glucose?

A

alpha-1,4 linkages.

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3
Q

What branches glucose chains?

A

alpha-1,6 linkages.

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4
Q

Why is glucose stored as glycogen in the cell?

A

Because glycogen has a low osmotic potential, meaning it doesn’t attract mass amounts of water. This is good as water won’t be pulled into the cell, causing it to swell and die.

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5
Q

Where does glycogen synthase add new units?

A

To the nonreducing end of glycogen.

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6
Q

What is glycogen phosphorylase regulated by?

A

It’s regulated by GPCR (s) in which adenylate cyclase is stimulated by glucagon/adrenaline to increase the levels of cAMP. This increases PKA, which phosphorylates and activates phosphorylase kinase. This molecule activates phosphprylase b to a.

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7
Q

What are the two forms of glycogen phosphorylase?

A

Phosphorylase b and a.

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8
Q

What is the difference in the activity of the two forms of glycogen phosphorylase?

A

Phosphorylase b exists in a low activity form, known as the T state whereas phosphorylase a is the high activity form, also known as the R state.

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9
Q

Is phosphorylase b only in the T state?

A

No it can exist in the R state as well; however, it’s more likely for phosphorylase a to dominate this stage.

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10
Q

What happens to the helices in glycogen phosphorylase when it’s phosphorylated?

A

In the low activity state these helices in the middle of the molecule are perpendicular; however when phosphorylated, these helices are rotated to expose the catalytic sites.

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11
Q

What stimulates the phosphorylation of phosphorylase b?

A
  1. Glucagon in the liver/adrenaline in the bloodstream
  2. Allosteric activation of AMP in the muscle (binding to phosphorylase b kinase)
  3. Increase in calcium in the muscle activates phosphorylase kinase
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12
Q

How to switch off glycogen synthase when the breakdown of glycogen is occuring?

A
  1. Same pathway that activates glycogen phosphorylase (GsPCR with adenylate cyclase stimulation)
  2. PKA phosphorylates glycogen synthase to gives its low activity enzyme configuration
    OR
  3. Glycogen synthase kinase-3 will phosphorylate glycogen synthase a at a different site with the same effect (turned to b form)
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13
Q

What does constitutively active mean?

A

That it’s always turned on.

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14
Q

What does protein phosphatase 1 do?

A
  1. Binds to a glycogen-targeting protein (GM)
  2. This brings PP1 and glycogen close together
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15
Q

Where is protein phosphatase 1 (PP1) present?

A

Skeletal muscle and the liver.

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16
Q

How is PP1 inhibited?

A

By phosphorylating the molecule through PKA.

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17
Q

Why does the phosphorylation of PP1 result in its inactivation?

A
  1. The dissociation of PP1 from its targeting complex (glycogen-binding region)
  2. Allows an inhibitor molecule to bind really tightly to the less active PP1
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18
Q

What does PP1 promote and inhibit?

A

It promotes glycogenesis and inhibits glycogenolysis.

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19
Q

What happens if you add glucose to the liver?

A

Rapidly change from a state where the phosphorylase is active to one where the synthase is fully active.

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20
Q

How does insulin effect PP1?

A
  1. Triggers phosphorylation of glycogen targeting protein at a different site (NOT PKA one)
  2. Activation of PP1
  3. Switch on glycogen synthase
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21
Q

How are lipids solubility in water?

A

Insoluble

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22
Q

What do lipids contain?

A

C, H, and O; phospholipids have P, N

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23
Q

Why do lipids have more energy than carbohydrates?

A

Because they are much more reduced, thus release of more energy when oxidized.

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24
Q

How do ketone bodies differ from lipids?

A

They are water soluble.

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25
Q

Can lipids travel in the bloodstream?

A

Not by themselves as they are hydrophobic.

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26
Q

How are lipids transported?

A

Using spherical lipoprotein particles.

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27
Q

What are lipoproteins made of?

A

Neutral core of TAGs and cholesterol esters; and an outer shell of phospholipids, free cholesterol, and apolipoproteins.

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28
Q

What is the role of chlyomicron?

A

Dietary fat transport

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29
Q

What is the role of VLDL?

A

Endogenous fat transport

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30
Q

What is the role of IDL?

A

LDL precursor

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31
Q

What is the role of LDL?

A

Cholesterol transport

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32
Q

What is the role of HDL?

A

Reverse cholesterol transport

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33
Q

How is cholesterol taken into a cell?

A
  1. LDL receptor synthesized in RER and moves to the plasma membrane
  2. LDL receptor binds the apoB-100 on LDL, initiating endocytosis
  3. LDL is internalized in an endosome
  4. LDL receptor is segregated into vesicles and recycled to the surface
  5. Endosomes with LDL fuse with the lysosome
  6. Lytic enzymes in lysosome degrade apoB-100 and cholesteryl esters, releasing aa, FA, and cholesterol
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34
Q

What proteins complement chylomicrons?

A

apoCII

35
Q

What does apoCII do?

A

It’s a cofactor that activates lipoprotein lipase (LPL) that lines lumenal walls of tissues to hydrolyse TAGs.

36
Q

Where is lipoprotein lipase usually found?

A

Associated with endothelial cells of capillary walls of adipose/muscle/cardiac; mainly present near tissues that need TAGs.

37
Q

What is a chylomicron remnant?

A

Ones that after TAG hydrolysis and apoB/apoCII removal.

38
Q

How to process a dietary lipid?

A
  1. Solubilize
  2. Breakdown
  3. Packaging and transport
  4. Release and uptake of cargoes at correct target tissues
39
Q

How to solubilize lipids?

A

Bile salts secreted by the pancreas solubilize lipids.

40
Q

What do lipases do?

A

Breakdown lipids into constituent FAs and MAGs.

41
Q

What happens to FAs and MAGs?

A

Easily diffuse across the cell membrane into mucosal cells where they are reformed back into TAGs.

42
Q

Where does chylomicron assembly begin? What is it called?

A

In the ER of intestinal epithelial cells, where they are known as nascent chylomicron.

43
Q

Where is the chylomicron matured? How?

A

In the lymph and blood when apoE and apoCII are added from HDL.

44
Q

What proteins are associated with chylomircon?

A

apoCII, apoE, and apoB-48.

45
Q

What does lipoprotein lipase hydrolyzes TAG into?

A

Glycerol and FFA

46
Q

What are FFAs used as?

A

By muscle cells or other tissues as fuel and used to re-esterify MAG in adipose to form stores of TAG.

47
Q

What is glycerol used as?

A

By the liver to produce glycerol 3-phosphate.

48
Q

Where does biosynthesis of fatty acids occur in the cell?

A

In the cytoplasm

49
Q

Where does biosynthesis of fatty acids occur in the boyd?

A

Liver and adipose tissue

50
Q

What does biosynthesis of fatty acids consume?

A

NADPH and ATP

51
Q

What are the intermediates in biosynthesis of fatty acids linked to?

A

Acyl carrier protein (ACP).

52
Q

What is the first step of fatty acid biosynthesis?

A

It’s the rate-limiting step in which acetyl CoA carboxylase performs the carboxylation of acetyl CoA to form malonyl CoA.

53
Q

How many carbons are added each cycle of fatty acid synthesis?

A

2 carbons

54
Q

How many NADPH consumed in a cycle of fatty acid synthesis?

A

2 NADPH

55
Q

What does fatty acid synthase do?

A

It’s a single polypeptide with 7 domains in which each domain catalyses a different reaction.

56
Q

When do want fatty acid synthesis to occur?

A

When there is a plentiful supply of energy, thus in the fed state when food is coming in.

57
Q

What hormone activates acetyl CoA carboxylase?

A

Insulin

58
Q

What hormone inhibits acetyl CoA carboxylase?

A

Glucagon and AMP

59
Q

How is acetyl CoA carboxylase inhibited?

A

By phosphorylation

60
Q

What phosphorylates acetyl CoA carboxylase?

A

AMP-activated protein kinase

61
Q

What dephosphorylates acetyl CoA carboxylase?

A

Protein phosphatase 2A

62
Q

What is the structure of the active acetyl CoA carboxylase?

A

Big, long polymers

63
Q

What is the structure of the inactive acetyl CoA carboxylase?

A

Dimerized

64
Q

What is an allosteric activator of acetyl CoA carboxylase?

A

Citrate

65
Q

What is an allosteric inhibitor of acetyl CoA carboxylase? What is this an example of?

A

Feedback inhibition via palmitoyl-CoA

66
Q

Where is acyl-CoA stored?

A

In the liver

67
Q

What happens to acyl-CoA in the liver when it’s increasing in concentration?

A

Packaged into VLDL

68
Q

Where is VLDL brought?

A

To the adipose tissue for storage

69
Q

What is lipoprotein lipase activated by?

A

Insulin

70
Q

What is activated during the fasted state for fatty acid breakdown?

A

ATGL (adipose triglyceride lipase)
HS lipase (hormone sensitive lipase)

71
Q

How are ATGL and HS lipase activated?

A
  1. Glucagon binds to GPCR
  2. G alpha s subunits dissociated and activates adenylate cyclase
  3. Increase in cAMP = increase in PKA activation
  4. Phosphorylation of perilipin, releases a co-activator protein
  5. CA activates ATGL
  6. PKA phosphorylates and activates HS lipase
72
Q

What does ATGL do?

A

Breaks down TAG to DAG

73
Q

What does HS lipase do?

A

Breaks down DAG to MAG.

74
Q

What does insulin do for fatty acid breakdown?

A

Slows the process down, thus resulting in the dephosphorylation of the intermediates.

75
Q

Where does beta oxidation occur?

A

In the mitochondria

76
Q

How much NADH and FADH2 is produced in beta-oxidation?

A

1 each

77
Q

How much carbons are removed during a cycle of beta-oxidation?

A

Two

78
Q

What are all intermediates linked to in beta-oxidation?

A

Coenzyme A

79
Q

What is the key regulatory step of FA oxidation?

A

When the FA coA is transferred from the cytosol to mitochondrial matrix using carnitine acyltransferase.

80
Q

What does carnitine acyltransferase do?

A
  1. Carnitine acyltransferase 1 is a carrier molecule that transfers acyl-CoA from cytosol to mitochondrial matrix
  2. Carnitine acyltransferase 2 catalyzes the reverse reaction to release the molecule

NO ENERGY

81
Q

What inhibits carnitine acyltransferase?

A

Malonyl-CoA, which was made in fatty acid synthesis.

82
Q

How to regulate beta oxidation?

A
  1. Inhibition of enzyme activity by high energy signals
    - beta-hydroxyacyl CoA dehydrogenase thiokinase
  2. Control of availability of FAs
    - insulin inhibits HSL and decreases rate of FA release
83
Q

How does malonyl-CoA regulate beta oxidation?

A
  1. When carboxylase is inactive, the concentration of malonyl CoA will drop (intermediate of FA synthesis), so the rate of FA oxidation increases
  2. Active fatty acid synthesis means active carboxylase and thus malonyl CoA decreases in concentration, and thus the rate of FA oxidation decreases

Protein Control in Cellular Regulation (8 decks)

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