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Biochem > Fatty acid oxidation > Flashcards

Fatty acid oxidation Flashcards

1
Q

Location where lipids are stored

A

Adipose

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2
Q

What has the highest energy per gram:
Carbs, amino acids, fats, or alcohol?

A

Fats

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3
Q

Energy content (in kcal/gm) of carbohydrates and amino acids

A

4

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4
Q

Energy content (in kcal/gm) of fats

A

9

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5
Q

Energy content (in kcal/gm) of alcohol

A

7

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6
Q

Are blood levels of free fatty acids high or low?

A

Low (fast turnover)

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7
Q

2 essential fatty acids

A

Linoleic acid
Alpha-linolenic acid

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8
Q

Precursor of prostaglandins

A

Arachidonic acid

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9
Q

Subcellular location where fat is burned

A

mitochondria

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10
Q

Fuel source preference for heart, liver, and muscle

A

Fat

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11
Q

Fuel source preference for brain and RBCs

A

Glucose

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12
Q

Time during fasting where glycogen supplies become depleted

A

16-24 hours

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13
Q

Oxidation of fatty acids to acetyl CoA provides energy for this process

A

gluconeogenesis

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14
Q

The energy for gluconeogenesis comes from

A

Oxidation of fatty acids to acetyl CoA

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15
Q

Source of most calories for the body under most conditions, including at rest, prolonged exercise, starvation, and long term starvation

A

Fatty acids

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16
Q

In a fasted state, liver oxidizes fat to form this, which it releases into the blood for use in other tissue

A

Ketone bodies

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17
Q

Enzyme that catalyzes the conversion of triglyceride to 3 fatty acids and glycerol

A

Hormone-sensitive lipase

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18
Q

Is Hormone-sensitive lipase active or inactive when phosphorylated?

A

Active

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19
Q

Is Hormone-sensitive lipase active in fed or fasted state?

A

Fasted state

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20
Q

Effect of insulin on Hormone-sensitive lipase

A

Inactivates via protein phosphatase 1

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21
Q

Effect of glucagon on Hormone-sensitive lipase

A

Activates/phosphorylates via cAMP/PKA pathway

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22
Q

Effect of epinephrine on Hormone-sensitive lipase

A

Activates/phosphorylates via cAMP/PKA pathway

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23
Q

Free fatty acids are transported to various tissues in the blood bound to this

A

Albumin

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24
Q

Glycerol produced in triacylglycerol degradation in adipocytes is transported to this organ for use in what process?

A

Transported to liver
For gluconeogenesis

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25
Q

The initial step of using glycerol for gluconeogenesis requires this enzyme that is absent/marginal in adipose and most other tissues except liver

A

Glycerol kinase

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26
Q

Glycerol kinase is present in this organ and absent/marginal in all others

A

Liver

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27
Q

Number of carbons in short chain fatty acid

A

4-6

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28
Q

Number of carbons in medium chain fatty acid

A

4-12

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29
Q

Number of carbons in long chain fatty acid

A

12-20

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30
Q

Number of carbons in very long chain fatty acid

A

20+

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31
Q

Long chain fatty acid oxidation is activated by addition of this

A

CoA

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32
Q

Activation of long chain fatty acids during oxidation occurs in this subcellular locatoin

A

ER or outer mitochondrial membrane

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33
Q

This is required for transport of C12 and longer fatty acids into the mitochondrial matrix

A

Activation by addition of CoA

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34
Q

Activation of long chain fatty acids by addition of CoA requires this

A

2 ATP equivalents used –> form Fatty acyl-CoA + AMP + PPi

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35
Q

Form of long chain fatty acids that can be transported through outer mitochondrial membrane but not the inner membrane

A

Fatty acyl CoA

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36
Q

This molecule replaces CoA on long chain fatty acids for transport across the inner mitochondrial membrane

A

Carnitine

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37
Q

Types of fatty acids that enter the mitochondria by simple diffusion and thus bypass the transport system

A

Short and medium chain

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38
Q

Type of fatty acid that cannot enter the mitochondrial matrix

A

Very long chain fatty acids

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39
Q

Since very long chain fatty acids cannot enter the mitochondrial membrane, they are transported here instead

A

Peroxisome

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40
Q

Peroxisome oxidation of very long chain fatty acids produces this from FADH2 by direct reaction with oxygen

A

H2O2

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41
Q

Enzyme that converts H2O2 to oxygen and water in the peroxisome

A

Catalase

42
Q

Transmembrane protein bound to the outer mitochondrial membrane that catalyzes:
Fatty acyl CoA + carnitine –> CoA + fatty acylcarnitine

A

Carnitine palmitoyl transferase I (CPT I)

43
Q

Carnitine palmitoyl transferase I (CPT I) is found in this subcellular location

A

Bound to the outer mitochondrial membrane

44
Q

The active site of Carnitine palmitoyl transferase I (CPT I) is in this subcellular location

A

Inter mitochondrial space (between the inner and outer mitochondrial membranes)

45
Q

Rate limiting step of oxidation of long chain fatty acids

A

Carnitine palmitoyl transferase I (CPT I)
(Transport into mitochondrial matrix)

46
Q

Inhibition of Carnitine palmitoyl transferase I (CPT I)

A

Malonyl coA

47
Q

Does high (ATP) or low (AMP) energy block malonyl coA formation

A

Low energy via AMP-dependent protein kinase (AMPK)

48
Q

Enzyme that is stimulated in low energy state (AMP) and shuts of malonyl CoA formation, allowing fatty acid transport and oxidation to occur.
Activates carb and fat catabolism

A

AMP-dependent protein kinase (AMPK)

49
Q

AMP-dependent protein kinase (AMPK) is found in these tissues

A

Muscle and liver

50
Q

Does NADH or NAD+ inhibit beta oxidation?

A

NADH
(NAD+ is required for beta oxidation)

51
Q

Is NADH or NAD+ needed for beta oxidation?

A

NAD+

52
Q

Beta oxidation in the mitochondrial matrix involves the removal of 2 carbons at a time as this molecule with formation of these 2 other molecules used for oxidative phosphorylation

A

Acetyl CoA
NADH and FADH2

53
Q

Number of ATP generated from each round of beta oxidation

A

4

54
Q

Structure in ETC for fatty acid oxidation

A

Complex II-like structure

55
Q

For fatty acids with an odd number of carbons, the last 3 carbons are released as this

A

Propionyl CoA

56
Q

Enzyme that catalyzes:
Propionyl CoA –> D-methylmalonyl CoA

A

Propionyl CoA carboxylase

57
Q

Carboxylase enzymes always require this molecule

A

Biotin

58
Q

Requirements of propionyl CoA carboxylase (3)

A

Biotin, ATP, CO2

59
Q

Enzyme that catalyzes:
D-methylmalonyl CoA –> L-methylmalonyl CoA

A

Racemase

60
Q

Enzyme that catalyzes:
L-methylmalonyl coA –> Succinate

A

Mutase

61
Q

Requirement of mutase

A

Vitamin B12

62
Q

Molecule that acts as an indicator of B12 deficiency

A

Methylmalonyl CoA

63
Q

Enzyme involved in beta oxidation that requires Vitamin B12

A

Mutase

64
Q

Is ATP yield higher from fatty acid oxidation or glucose?

A

Fatty acids

65
Q

Configuration of fatty acid double bond on the beta carbon that is naturally occurring

A

cis

66
Q

Configuration of fatty acid double bonds on the beta carbon that is required for mitochondrial oxidation

A

trans

67
Q

Condition involving the absence of peroxisomes and accumulation of very long chain fatty acids

A

Zellweger syndrome

68
Q

Most severe form of peroxisomal biogenesis diseases
Patients usually die by 6 months of age

A

Zellweger syndrome

69
Q

X-linked metabolic disorder associated with an inability to transport saturated very long chain fatty acids into peroxisomes, resulting in accumulation of VLCFAs

A

Adrenoleukodystrophy (ALD)

70
Q

Process in peroxisomes needed to oxidize chlorophyll

A

Alpha oxidation

71
Q

Absence of alpha hydroxylase for alpha oxidation of chlorophyll in peroxisomes causes this condition

A

Refsum’s disease

72
Q

Alpha oxidation in peroxisomes is necessary to oxidize this

A

Chlorophyll

73
Q

Breakdown product from chlorophyll that requires alpha oxidation initially, removing the terminal carboxyl group as CO2 so that beta oxidation can then proceed normally

A

Phytanic acid

74
Q

Rare autosomal recessive defect in alpha-hydroxylation of phytanic acid, a breakdown product from chlorophyll

A

Refsum’s disease

75
Q

Process of formation of dicarboxylic acids

A

Omega oxidation

76
Q

Oxidation at the distal end of fatty acids produces this

A

Dicarboxylic acids

77
Q

This type of molecule is elevated in fatty acid disorders and deficiencies since beta oxidation does not work properly

A

Dicarboxylic acids
(since omega oxidation is done instead)

78
Q

The levels of these molecules are decreased in fatty acid disorders due to less fatty acid oxidation occurring

A

Ketone bodies
(less acetyl CoA produced to form ketone bodies)

79
Q

Only organ that produces ketone bodies

A

Liver

80
Q

Condition that differentiates fatty acid disorders from other metabolic disorders that cause hypoglycemia

A

Hypoketosis

81
Q

Are ketone bodies produced when oxaloacetate concentrations are high or low?

A

Low
(are used for gluconeogenesis)

82
Q

Does fasted or fed state produce more ketone bodies?

A

Fasted state (also high protein low carb diet)

83
Q

3 ketone bodies

A

Acetoacetate
Beta-hydroxy-butyrate
Acetone

84
Q

Enzyme that catalyzes:
3 Acetyl CoA → beta-hydroxy-beta-methyl glutaryl CoA (HMG CoA)

A

HMG CoA synthase

85
Q

Enzyme that catalyzes:
HMG CoA → Acetyl CoA + Acetoacetate

A

HMG CoA lyase

86
Q

Acetoacetate is reduced to beta-hydroxy-butyrate (BHB) in this subcellular location

A

Mitochondria

87
Q

Equilibrium between Acetoacetate and beta-hydroxy-butyrate in the mitochondria is determined by this

A

Ratio of NAD+ to NADH
AcAc + NADH ↔ BHB + NAD+

88
Q

Nonenzymatic, spontaenous decarboxylation of acetoacetate produces this two molecules

A

Acetone + CO2

89
Q

Molecule used as a diagnostic tool for unregulated diabetes since it is a marker of ketosis
Involves fruity breath

A

Acetone

90
Q

Source of CoA which is transferred to Acetoacetone via a transferase enzyme that is absent in the liver

A

Succinyl CoA

91
Q

Enzyme that catalyzes:
Acetoacetyl CoA –> 2 acetyl CoA

A

Thiolase

92
Q

Levels of ketone bodies, pH, and glucose in a type 1 diabetic not taking insulin

A

Extreme levels of ketone bodies
Acidosis
Hyperglycemia

93
Q

Low carb high protein diet stimulates this state

A

Fasted; promotes ketosis

94
Q

Compound elevated in the fasting state due to break down of muscle protein into free amino acids

A

Urea

95
Q

MCAD deficiency involves a lack of this enzyme activity

A

Medium chain acyl CoA dehydrogenase

96
Q

Effect of glucose levels and ketone bodies in MCAD deficiency

A

Hypoglycemia
Reduced ketone body formation under fasting conditions

97
Q

Genetic condition caused by lack of medium chain acyl CoA dehydrogenase activity

A

MCAD deficiency

98
Q

Genetic condition caused by lack of long chain acyl CoA dehydrogenase activity, leading to hypoglycemia

A

LCAD deficiency

99
Q

Condition caused by inhibition of carnitine activity by hypoglycin
Can lead to death because of severe hypoglycemia

A

Jamaican vomiting disorder

100
Q

Jamaican vomiting disorder involves inhibition of this by hypoglycin

A

Carnitine

Biochem (21 decks)

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