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Biochem 2 (CHEM 441B) > Ch. 16 > Flashcards

Ch. 16 Flashcards

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1
Q

What purposes do fatty acid oxidation and fatty acid synthesis serve in animals?

A
  • Fatty acid oxidation: provides energy to cells when glucose levels are low
  • Fatty acid synthesis: liver and adipose tissue convert excess acetyl-CoA into fatty acids that can be stored or exported as TAGs
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2
Q

What are the net reactions of fatty acid degradation and synthesis for the typical C16 fatty acid palmitate?

A
  • Fatty acid oxidation

Palmitate + 7 NAD+ + 7 FAD + 8 CoA + 7 H2O + ATP –> 8 Acetyl-CoA + 7 NADH + 7 FADH2 + AMP + 2 Pi + 7 H+

  • Fatty acid synthesis

8 Acetyl-CoA + 7ATP + 14 NADPH + 14 H+ –> Palmitate + 8 CoA + 7 ADP + 7 Pi + 14 NADP+ + 6 H2O

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3
Q

What are the key enzymes in fatty acid metabolism?

A
  • Fatty acyl-CoA synthetase
  • Carnitine acyltransferase I (CAT1)
  • Acetyl-CoA carboxylase
  • Fatty acid synthase
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4
Q

What are examples of fatty acid metabolism in everyday biochemistry?

A

Kangaroo rat and camel: survive in deserts for long periods of time without drinking water

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5
Q

What is fatty acyl-CoA synthetase?

A

Set of 3 enzymes responsible for formation of fatty acyl-CoA molecules
- Catalyzes priming reaction

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6
Q

What is carnitine acyltransferase I (CAT1)?

A

Mitochondrial outer membrane enzyme that converts fatty acyl-CoA to fatty acyl-carnitine for transport into mitochondria

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7
Q

What is acetyl-CoA carboxylase?

A

Cytosolic enzyme that carboxylates acetyl-CoA
- 1st step in fatty acid synthesis (commitment step)

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8
Q

What is fatty acid synthase?

A

Multi-functional protein (euks) or multienzyme complex (proks) that’s responsible for synthesis of fatty acids like palmitate

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9
Q

Where does fatty acid β-oxidation occur?

A

Mitochondria

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10
Q

What are the steps of the formation of fatty acyl-CoA?

A
  1. Fatty acyl-CoA synthetase catalyzes the adenylation of a fatty acid to form fatty acyl-adenylate (enzyme-bound
    intermediate)
  2. Fatty acyl-adenylate is attacked by the thiol group of CoA, forming the thiolester fatty acyl-CoA product and releasing AMP
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11
Q

What are the 2 possible fates of fatty acyl-CoA? (hint: has to do with energy charge)

A
  1. Low energy charge: fatty acid degradation is favored
  2. High energy charge: fatty acid synthesis is favored
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12
Q

What is the carnitine transport cycle?

A

3-step process that translocates fatty acids across the inner mitochondrial membrane

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13
Q

What is this?

A

Carnitine

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14
Q

What are the steps of the carnitine transport cycle?

A
  1. CAT1 replaces CoA with carnitine to form palmitoylcarnitine
    - Inhibited by malonyl-CoA when fatty acid synthesis is favored
  2. Carnitine-acetylcarnitine translocase exchanges palmitoylcarnitine for carnitine
  3. Conversion of palmitoylcarnitine back to palmitoyl-CoA
    - Catalyzed by CAT2
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15
Q

What are the 2 important functions of the carnitine transport cycle in regulating cell metabolism?

A
  1. Provides mechanism to control flux of fatty acids into degradation or TAG/membrane lipid synthesis
  2. Maintains separate pools of CoA (cytosolic and mitochondrial)
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16
Q

What is the β-oxidation pathway?

A

Fatty acid oxidation pathway that removes 2-carbon units from a fatty acid chain
- Produces FADH2, NADH, and acetyl-CoA

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17
Q

What is hypoglycin A?

A

Amino acid derivative found in high concentrations in unripe ackee fruit
- Inhibitor of liver mitochondrial acyl-CoA dehydrogenases
- Jamaican vomiting sickness

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18
Q

What is the net reaction of the β-oxidation pathway?

A

Palmitoyl-CoA + 7 CoA + 7 FAD + 7 NAD+ + 7 H2O –> 8 Acetyl-CoA + 7 FADH2 + 7 NADH + AMP + 2 Pi + 7 H+

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19
Q

What are the steps of electron transfer in β-oxidation?

A
  1. Acyl-CoA dehydrogenase donates electrons from the first fatty acid oxidation reaction to enzyme-bound FAD in ETF
  2. Electron pair is passed to Fe-S center in ETF-Q oxidoreductase
  3. Electron pair is passed from Fe-S center to coenzyme Q
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20
Q

What are the auxiliary pathways for fatty acid oxidation?
Note: β-oxidation usually uses even-numbered and fully saturated fatty acids

A
  • Degradation of monounsaturated fatty acids (ex. oleoyl-CoA)
  • Degradation of unsaturated fatty acids (ex. cis-Δ9, cis-Δ12-linoleoyl-CoA
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21
Q

What is ketogenesis? Where does it occur?

A
  • Conversion of excess acetyl-CoA into ketone bodies
  • Liver cell mitochondria
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22
Q

List ketone bodies.

A

Acetoacetate and D-β-hydroxybutyrate

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23
Q

What are the steps of ketogenesis?

A
  1. β-ketoacyl-CoA thiolase condenses 2 molecules of acetyl-CoA to form acetoacyl-CoA
  2. HMG-CoA synthase adds another acetyl-CoA to form HMG-CoA
  3. HMG-lyase converts HMG to acetoacetate
    4 & 5. Acetoacetate is exported directly or converted to acetone
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24
Q

What uses ketone bodies to generate acetyl-CoA?

A
  • Skeletal and cardiac muscle
  • During extreme starvation: brain
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25
Q

What is ketoacidosis?

A

Side effect of excess ketone body formation, resulting in low blood pH

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26
Q

Diagram the carbon flow from glucose to fatty acids.

A
  1. Citrate synthase combines oxaloacetate and acetyl-CoA to form citrate, which is shuttled to the cytosol where it is cleaved by citrate lyase back into acetyl-CoA and oxaloacetate
  2. Cytosolic acetyl-CoA is converted to malonyl-CoA by acetyl-CoA carboxylase
  3. Liver cells: fatty acids and glycerol are combined to form TAGs, which are packed in VLDLs
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27
Q

What is citrate lyase?

A

Cytosolic enzyme that cleaves the acetyl group from citrate to form acetyl-CoA and oxaloacetate

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28
Q

Fatty acid synthesis and degradation are complementary pathways. Compare and contrast them.

A

Both
- Require 4-step reaction cycle
- Involve removal or addition of C2 units attached to CoA

Differences prevent futile cycling
- Different locations
- Different reductants/oxidant
- Degradation needs multiple enzymes but synthesis only needs 1 multifunctional enzyme
- Degradation uses CoA as acetyl group anchor vs. synthesis uses ACP as hydrocarbon anchor

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29
Q

What is ACP?

A

Protein with serine linked phosphopantetheine group that serves as the attachment site for intermediates during fatty acid synthesis

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30
Q

Where does fatty acid degradation occur?

A

Mitochondrial matrix

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31
Q

What are the oxidants for fatty acid degradation?

A

FAD and NAD+

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32
Q

What is the rate-limiting step for fatty acid degradation?

A

Carnitine-mediated transport into the mitochondrial matrix

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33
Q

Where does fatty acid synthesis occur?

A

Cytosol

34
Q

What is the reductant for fatty acid synthesis?

A

NADPH

35
Q

What is the rate-limiting step for fatty acid synthesis?

A

Generation of malonyl-CoA

36
Q

What are the 3 activities of acetyl-CoA carboxylase?

A
  1. Biotin carboxylase
  2. Biotin carrier
  3. Carboxyltransferase
37
Q

What are the 4 conserved reactions of fatty acid synthesis?

A
  1. Condensation
  2. Reduction
  3. Dehydration
  4. Reduction
38
Q

Info on mammalian fatty acid synthase

A
  • ~2500 amino acids (~275 kDa)
  • 7 protein functions encoded in a single polypeptide chain
  • Dimeric protein with each monomer containing 2 functional lobes
    • Upper lobe contains the 3 modifying functions (KR, DH, ER)
    • Lower lobe contains the 2 condensing functions (KS, MAT)
39
Q

What is the net reaction of fatty acid synthesis?

A

8 Acetyl-CoA + 7 ATP + 14 NADPH + 14 H+ –> Palmitate + 8 CoA

40
Q

Where do the enzymes that elongate palmitate exist?

A

Mitochondria and as membrane components of the ER

41
Q

What are mixed-function oxidases?

A

Group of desaturating enzymes that convert fatty acyl-CoA into longer fatty acids
- Membrane-bound ER proteins that use molecular oxygen (O2) as oxidant

42
Q

What is the citrate shuttle?

A

Mechanism for transporting acetyl-CoA groups (via citrate) from mitochondria to cytosol
- Provides mechanism to stimulate fatty acid synthesis in the cytosol when acetyl-CoA accumulates in the mitochondria (buildup occurs when glucose levels are high and the citrate cycle is feedback-inhibited by high energy charge in cell)

43
Q

What is the primary control point of fatty acid synthesis?

A

Modulation of acetyl-CoA carboxylase activity

44
Q

In what form is acetyl-CoA carboxylase active?

A

Hompolymer

45
Q

What activates acetyl-CoA carboxylase?

A

Citrate

46
Q

What inactivates acetyl-CoA carboxylase?

A

Palmitoyl-CoA

47
Q

How is fatty acid synthesis hormonally controlled?

A

Shifts equilibrium between polymeric and monomeric forms as a function of phosphorylation state
- Phosphorylated by glucagon: monomeric (inactive)
- Dephosphorylated by insulin: polymeric (active)

48
Q

What is AMPK?

A

AMP-sensitive regulatory protein that functions as a key regulator of numerous metabolic pathways, including fatty acid synthesis

49
Q

What is AMPK activated by?

A

Lower energy charge (high AMP)

50
Q

What regulates AMPK activity?

A

AMP-binding (induces conformational change, facilitating its phosphorylation at a regulatory threonine residue)

51
Q

How are fatty acid synthesis and degradation allosterically controlled by metabolites?

A
  1. Feedback inhibition of the citrate cycle under high energy charge leads to citrate export to cytosol, where it stimulates activation of acetyl-CoA carboxylase (citrate in cytosol promotes synthesis)
  2. High levels of malonyl-CoA inhibit CAT1, which prevent mitochondrial import and degradation of fatty acyl-CoA molecules at the same time that fatty acid synthesis is favored (malonyl-CoA inhibits degradation)
  3. High levels of faty acyl-CoA inhibit acetyl-CoA carboxylase by fatty acyl-CoA binding (fatty acyl-CoA inhibits synthesis)
52
Q

What is LDL?

A

Class of cholesterol-transporting molecules that moves cholesterol from liver through blood to
peripheral tissue

53
Q

What is cholesterol synthesized from?

A

Acetyl-CoA

54
Q

Is cholesterol an essential lipid?

A

No, because of de novo synthesis

55
Q

What is Stage 1 of cholesterol biosynthesis?

A

Generation of mevalonate from acetyl-CoA

56
Q

What is Stage 2 of cholesterol biosynthesis?

A

Conversion of mevalonate to isopentanyl pyrophosphate dimethylallyl
pyrophosphate

57
Q

What is Stage 3 of cholesterol biosynthesis?

A

Formation of squalene from 4 isopentanyl pyrophosphates & 2 dimethylallyl
pyrophosphates

58
Q

What is Stage 4 of cholesterol biosynthesis?

A

Cyclization of squalene & lanosterol modification to form cholesterol

59
Q

What is mevalonate?

A

Intermediate in cholesterol biosynthesis, formed by the condensation of 3 acetyl-CoA molecules

60
Q

What is HMG-CoA reductase?

A

Enzyme responsible for formation of mevalonate from
acetyl-CoA

61
Q

What are the 3 steps of Stage 1 of cholesterol biosynthesis?

A
  1. 2 acetyl-CoA condensed to form acetoacetyl-CoA
  2. 3rd acetyl-CoA added to form HMG-CoA
  3. Rate-limiting step: HMG-CoA reductase converts
    HMG-CoA to mevalonate in reduction reaction that
    uses 2 NADPH releases CoA
62
Q

What are the 3 primary functions of cholesterol?

A

If esterified…
- Stored in intracellular lipid droplets
- Packaged into lipoproteins and exported into circulatory system
- Secreted into small intestine or bile duct during digestion

63
Q

What is cholate?

A

Major bile acid formed in liver by conversion of cholesterol

64
Q

What are the major classes of lipoproteins?

A
  • Chylomicrons
  • VLDL
  • IDL
  • LDL
  • HDL
65
Q

All lipoproteins consist of…

A
  • Phospholipid monolayer
  • 1 or more apolipoproteins on the surface (serve as signal molecules that activate enzymes or bind to cell surface receptors)
66
Q

What is HDL?

A

Class of cholesterol-transporting molecules that transport cholesterol from peripheral tissues to liver

67
Q

What determines the steady-state levels of circulating cholesterol?

A

The balance of cholesterol input (diet and de novo synthesis), cholesterol recycling (returning tissue cholesterol to liver), and cholesterol output (loss of bile acids by excretion)

68
Q

What does LDL transport cholesterol to?

A

From liver to peripheral tissues and arteries

69
Q

What does HDL transport cholesterol to?

A

From peripheral tissues and arteries to liver

70
Q

How do HDL particles function in reverse transport?

A
  1. apoA-I activates lecithin-cholesterol acyltransferase
  2. Lecithin-cholesterol acyltransferase esterifies cholesterol
  3. HDL takes up cholesterol esters
  4. HDL transports cholesterol back to liver
71
Q

What is atherosclerosis?

A

Arterial blockage due to accumulation of fibrous tissue (rich in cholesterol, fat, a foam cells) in arterial walls

72
Q

What is a myocardial infarction?

A

Heart attack

73
Q

What is coronary artery bypass surgery?

A

Surgical procedure where veins are grafted to ther myocardium to restore blood flow to regions of the heart suffering from decreased oxygen due to atherosclerosis

74
Q

What is familial hypercholesterolemia (FH)?

A

Recessive genetic disorder where individuals have reduced numbers of LDL receptors, resulting in high levels of serum LDL and associated cardiovascular disease

75
Q

What happens if a person has mutations in both copies of the LDL receptor gene?

A
  • No LDL receptors on cell surface
  • Serum LBL levels are 5x higher than normal
  • Severe atherosclerosis
  • Die of heart attacks or strokes in early childhood
76
Q

What happens if a person has only 1 mutant LDL receptor gene?

A
  • Serum LDL IeveIs are 2-3x higher than normal
  • Often have 1st heart attack before 30
77
Q

What are the biochemical processes by which LDL receptors control serum LDL levels?

A
  • LDL binds to receptor through apoB-100 occurs at specific sites in PM (clathrin-coated
    pits)
  • Low cholesterol levels stimulate HMG-CoA reductase activity
78
Q

What are statin drugs?

A

Class of drugs that bind to and inhibit HMG-CoA reductase, indirectly resulting in decreased serum cholesterol levels and decreased risk of cardiovascular disease

79
Q

What is the benefit of statin-mediated inhibition of HMG-CoA reductase activity?

A

Indirect effect of stimulating LDL receptor expression through activation of SREBP
- Lowering cholesterol levels in the liver –> LDL receptor expression is stimulated, resulting in elevated LDL endocytosis and a concomitant decrease in atherosclerotic disease

80
Q

What are sterol regulatory element binding proteins (SREBPs)?

A

Dimeric DNA-binding protein that binds to SREs & regulates gene expression

81
Q

Flux through lipid metabolism is regulated based on what 3 cellular demands?

A
  1. Changing energy needs of the cell
  2. Requirement for membrane components in rapidly dividing cells
  3. Need to synthesize cholesterol derivatives
82
Q

How are precursor SREBPs activated?

A

Biochem 2 (CHEM 441B) (23 decks)

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