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BIOS4007 - Bioenergetics and Primary Metabolism > Lipid Metabolism > Flashcards

Lipid Metabolism Flashcards

1
Q

What is the fatty acid synthesis pathway?

A

Involves a series of enzymatic reactions that ultimately lead to the production of fatty acids

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2
Q

What are some basic functions of lipids in cells?

A

Lipids play a wide range of functions in cells, including:
- energy storage
- structural roles
-insulation (electrical & thermal)
- surfactant
- signalling molecules

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3
Q

What are some examples of lipids as signalling molecules?

A
  • hormones (e.g. steroids, leukotrienes)
  • intracellular messengers (e.g. DAG)
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4
Q

What is the simplest form of a lipid?

A
  • a fatty acid
  • general structure = R-COOH, where R is a hydrocarbon chain of 5-36 carbons
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5
Q

What are some other forms of lipids?

A
  • triacylglycerols as a storage form (also known as “fat”)
  • phospholipids in cell membranes
  • sphingolipids in the brain
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6
Q

How are fatty acids built up?

A

From successive additions of 2C units, which are derived from acetyl-CoA

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7
Q

Where are fatty acids synthesized?

A

Fatty acids are synthesized in the cytoplasm

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8
Q

How do acetyl-CoA molecules get from the mitochondria to the cytoplasm for fatty acid synthesis?

A
  • acetyl-CoA → citrate in mitochondria
  • then transported to the cytoplasm
  • where it is converted back to acetyl-CoA & used for fatty acid synthesis
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9
Q

What is the actual molecule used to add 2C units in fatty acid synthesis?

A

malonyl-CoA

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10
Q

What is the main regulated step in fatty acid synthesis?

A

Acetyl CoA carboxylase is the main regulated step in fatty acid synthesis

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11
Q

What is the function of acetyl CoA carboxylase in fatty acid synthesis?

A

An enzyme that converts acetyl-CoA → malonyl-CoA

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12
Q

What is the equation of the conversion of acetyl-CoA to malonyl-CoA?

A

acetyl-CoA + ATP + HCO3- → malonyl-CoA + ADP + Pi + H+

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13
Q

What is the substrate in the first step of fatty acid synthesis?

A

malonyl ACP

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14
Q

What type of reactions occur after the first step of fatty acid synthesis (in order)?

A
  • condensation
  • reduction
  • dehydration
  • reduction
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15
Q

What is the 2nd condensation reaction/step of fatty acid synthesis?

A

butyryl ACP + malonyl ACP → acetoacetyl ACP

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16
Q

What is the enzyme involved in the 2nd condensation reaction of fatty acid synthesis?

A

acyl-malonyl-ACP (condensing enzyme)

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17
Q

What is the reduction reaction/step of fatty acid synthesis?

A

acetoacetyl ACP → D-3-hydroxybutyryl ACP

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18
Q

What is the dehydration reaction step of fatty acid synthesis?

A

D-3-hydroxybutyryl ACP → crotonyl ACP

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19
Q

What is the 2nd reduction reaction of fatty acid synthesis?

A

crotonyl ACP → butyryl ACP

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20
Q

What are the energy requirements for FA synthesis?

A
  1. Acetyl-CoA + 7 malonyl-CoA + 14 NADPH + 20 H+ → Palmitate + 7 CO2 + 14 NADP+ + 8 CoA + 6H2O
  2. 7 Acetyl-CoA + 7 CO2 + 7 ATP → 7 Malonyl-CoA + 7 ADP + 7 Pi + 14 H+
  3. Overall equation:
    8 Acetyl-CoA + 7 ATP + 14 NADPH + 6 H+ → Palmitate + 14 NADP+ + 8 CoA + 6H2O + 7 ADP + 7 Pi
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21
Q

What is the length and saturation level of the fatty acid produced by fatty acid synthase?

A

C16, and it is fully saturated

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22
Q

What is the general length of most fatty acids?

A

Most fatty acids are longer than C16, with C20, C22, and C24 being the most common lengths

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23
Q

Where does the elongation of fatty acids occur?

A

elongated in the smooth endoplasmic reticulum (ER)

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24
Q

What carbon is the most common site of desaturation in fatty acids?

A

C9

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25
Q

Can mammals desaturate fatty acids beyond C9?

A

No

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26
Q

Are there essential fatty acids that must be obtained from the diet?

A

Yes, there are essential fatty acids that mammals cannot synthesize and must be obtained from the diet

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27
Q

What is the storage form of fatty acids in the body?

A

triacylglycerols

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28
Q

What is the advantage of using triacylglycerols for energy storage?

A

They are a high-density form of energy storage

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29
Q

Where are triacylglycerols made in the body?

A

Triacylglycerols are made in the liver

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30
Q

How are triacylglycerols transported around the body in circulation?

A

Triacylglycerols are transported around the body in circulation with proteins as lipoproteins

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31
Q

Where are triacylglycerols stored in the body?

A

Stored in adipocytes to form white fat

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32
Q

What are the different types of lipoproteins?

A
  • chylomicrons
  • VLDLs, IDLs, LDLs, and HDLs
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33
Q

What is the function of chylomicrons?

A

Chylomicrons are the largest (>400kDa) lipoproteins
function: transport dietary TAGs & cholesterol from the intestine to muscle/adipose

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34
Q

Where are VLDLs, IDLs, and LDLs synthesised?

A

Synthesized in the liver

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35
Q

What is the function of VLDLs, IDLs, and LDLs?

A

To transport lipids to muscle/adipose

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36
Q

What is the function of HDLs?

A

to transport lipids/cholesterol to the liver, where excess cholesterol is excreted in bile

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37
Q

Where are HDLs synthesized?

A

HDLs are made in plasma

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38
Q

Why are LDLs considered ‘bad’ and HDLs considered ‘good’?

A
  • LDLs are considered ‘bad’ as they can contribute to the development of atherosclerosis
  • HDLs are considered ‘good’ as they scavenge lipids & have a protective effect against atherosclerosis
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39
Q

What is the starting molecule for the formation of triacylglycerols?

A

dihydroxyacetone phosphate (DHAP)
- a glycolysis intermediate

40
Q

How is DHAP converted to glycerol-3-phosphate during triacylglycerol formation?

A

By generating NADH

41
Q

What is the first intermediate formed during triacylglycerol formation?

A
  • 2 FA chains are added to glycerol-3-phosphate
  • to give phosphatidic acid
  • which is the first intermediate formed during triacylglycerol formation
42
Q

How is diacylglycerol formed during triacylglycerol formation?

A
  • the phosphate group is removed from phosphatidic acid
  • to give diacylglycerol during triacylglycerol formation
43
Q

What is the final step in the formation of triacylglycerols?

A

The addition of a final FA chain to diacylglycerol

44
Q

What are the advantages of fat storage over glycogen storage?

A
  • fat has a higher energy content compared to glycogen, about 2.5-fold on complete oxidation
  • unlike glycogen, fat is not hydrated, resulting in a total of ~4-fold more energy per gram dry weight
45
Q

Are there any disadvantages to fat storage compared to glycogen storage?

A
  • while fat stores are not limited, they can expand with food intake, which can lead to obesity & related health issues
  • metabolism of fat is slower, making it better suited for longer-term storage rather than quick energy needs
46
Q

How is triacylglycerol synthesis regulated by hormones?

A

insulin stimulates the synthesis of triacylglycerol

47
Q

What are the different types of fat cell?

A
  • white
  • brown
48
Q

What else can acetyl-CoA be turned into?

A

cholesterol and its derivatives, e.g. vitamin D, steroid hormones, bile acids

49
Q

Can FAs generate signalling molecules?

A

Yes, FAs can generate signalling molecules

50
Q

What are some examples of signalling molecules that can be generated from FAs?

A

arachidonic acid: component of membrane phospholipids that is released when broken down by phospholipase A2

further broken down to:
- PGG2 → PGH2 (prostaglandins)
- 5-HPETE → leucotrienes
(slide 16)

51
Q

What are examples of PGH2 and its functions?

A
  • prostacyclins
  • prostaglandins
  • thromboxanes
  • inflammation, pain, gastroprotective PGs
52
Q

What are some examples of Leucotriene A4 and its functions?

A
  • leucotriene B4
  • cysteinyl leucotrienes
  • allergy, inflammation, gastric damage
53
Q

How are TAG broken down?

A
  • adrenaline & glucagon activate hormone sensitive lipase enzyme
  • TAG → free FAs + glycerol
54
Q

What is β-oxidation of FAs?

A

Metabolic pathway:
- that breaks down fatty acids into acetyl-CoA
- which can then enter the citric acid cycle & generate ATP

55
Q

What is the importance of β-oxidation in metabolism?

A
  • it is a major pathway for the breakdown of fatty acids
  • this pathway allows the body to generate ATP from stored fat when glucose is not available
56
Q

What is the reverse problem of FA synthesis in β-oxidation of FAs?

A
  • fatty acids need to be transported into the mitochondrial matrix
  • in order to be broken down through β-oxidation
57
Q

Why is it necessary to transport FAs into the mitochondrial matrix for β-oxidation?

A

Because this is where the enzymes required for β-oxidation are located

58
Q

Are all fatty acids fully saturated?

A

No, not all fatty acids are fully saturated

59
Q

What happens during β-oxidation when an unsaturated fatty acid has a double bond between C3 and C4?

A

β-oxidation will continue as normal until the double bond is reached, at which point it will stop

60
Q

What is the role of isomerase in the breakdown of unsaturated fatty acids?

A

Isomerase moves the double bond in an unsaturated fatty acid to a position between C2 and C3, allowing β-oxidation to continue

61
Q

Will β-oxidation continue after the role of isomerase in the breakdown of unsaturated fatty acids?

A

Yes, β-oxidation will continue after isomerase moves the double bond in an unsaturated fatty acid to a position between C2 and C3

62
Q

What happens during the breakdown of odd carbon fatty acid chains?

A

Successive rounds of β-oxidation will continue as normal until the final round

63
Q

What are the final products of the breakdown of odd carbon fatty acid chains?

A

acetyl-CoA and propionyl-CoA (C3)

64
Q

What happens to propionyl-CoA in the breakdown of odd carbon fatty acid chains?

A

Propionyl-CoA → succinyl-CoA

65
Q

What is methylmalonic acidosis?

A

A condition where the body is unable to breakdown propionyl-CoA → succinyl-CoA

66
Q

What is methylmalonic acidosis caused by?

A

Either:
- enzyme deficiency
- lack of coenzyme (deoxyadenosylcobalamin, a vitamin B12 derivative)

67
Q

What are the symptoms of methylmalonic acidosis?

A

Includes neurological issues such as:
- seizures
- encephalopathy
- stroke

68
Q

Is methylmalonic acidosis fatal if left untreated?

A

Yes, methylmalonic acidosis is fatal if left untreated

69
Q

What are the treatments for methylmalonic acidosis?

A

Includes
- a low protein diet
- (in severe cases) liver or kidney transplant

70
Q

Fates of acetyl-CoA from FA breakdown

A
  • sterols (cholesterol) & FAs
  • TCA cycle (aka citric acid cycle)
  • ketone bodies
  • protein acetylation (protein modification)
71
Q

What molecules does the intrinsic regulation of fat metabolism include?

A
  • citrate
  • palmitoyl CoA
  • malonyl CoA
72
Q

What is the intrinsic regulation of fat metabolism?

A
  • ↑ in citrate leads to an ↑ in fat synthesis
  • while ↑ in palmitoyl CoA leads to ↓ in fat synthesis
  • ↑ in malonyl CoA leads to ↓ in β-oxidation
73
Q

What is the extrinsic regulation of fat metabolism?

A

Involves the effects of hormones such as insulin and glucagon

74
Q

How does insulin regulate fat metabolism?

A

Insulin promotes fat synthesis and storage by:
- activating the enzymes involved in fat synthesis
- inhibiting those involved in fat breakdown

75
Q

How does glucagon regulate fat metabolism?

A

Glucagon promotes fat breakdown & energy production by:
- activating the enzymes involved in β-oxidation
- inhibiting those involved in fat synthesis

76
Q

Is all fatty acid breakdown carried out in the mitochondria?

A

No, not all fatty acid breakdown is carried out in the mitochondria - can also occur in peroxisomes

77
Q

What is the role of peroxisomes in fatty acid breakdown?

A

Peroxisomes are involved in the breakdown of fatty acids and produce H2O2 as a byproduct

78
Q

What is the role of H2O2 in peroxisomal fatty acid breakdown?

A
  • H2O2 is produced during peroxisomal fatty acid breakdown
  • is involved in oxidizing phenols and alcohols
79
Q

Why is peroxisomal fatty acid breakdown important in liver function?

A

Because it plays a key role in liver detoxification processes

80
Q

slides 22-26

A
81
Q

What is medium chain acyl-CoA dehydrogenase (MCAD) deficiency?

A

Genetic disorder that affects fatty acid metabolism
- most common fatty acid oxidation disorder
- affecting approximately 1 in 20,000 newborns

82
Q

What are the symptoms of MCAD deficiency?

A
  • lethargy
  • seizures
  • coma
  • hypoketotic hypoglycemia during fasting
83
Q

Is there a screening test available for MCAD deficiency?

A

Yes, there is a neonatal screening test available for MCAD deficiency

84
Q

What is long chain acyl-CoA dehydrogenase (LCAD) deficiency?

A

LCAD deficiency is a genetic disorder that affects fatty acid metabolism
- less common than MCAD deficiency
- affecting approximately 1 in 50,000 newborns

85
Q

What are the range of symptoms of LCAD deficiency?

A

Range from benign to fatal

86
Q

mk

A

nk

87
Q

What are the range of symptoms of VLCAD deficiency?

A

Range from benign to fatal

88
Q

What is carnitine deficiency?

A

The inability to synthesize carnitine & transport across epithelia
- it has been linked to autism in males

89
Q

What can carnitine deficiency lead to?

A
  • muscle cramping
  • severe weakness
  • even death
90
Q

What are the carnitine deficiences?

A
  • carnitine acyltransferase
  • carnitine/acylcaritine translocase
91
Q

What does carnitine acyltransferase deficiency lead to?

A
  • muscle weakness on exercise
  • as short-chain fatty acids can enter the mitochondrial matrix unaided
92
Q

What is atherosclerosis?

A

Atherosclerosis is a condition where:
- high levels of cholesterol (LDLs) can lead to the formation of plaques in the walls of arteries
- these plaques can break off or cause blood clots to form

93
Q

How can atherosclerosis be treated?

A

Treated by
- restricting dietary cholesterol intake
- taking medications such as statins, which can help lower cholesterol levels in the blood
- other treatments may include lifestyle changes such as exercise & quitting smoking

94
Q

What are the consequences of atherosclerosis?

A

Include:
- heart attacks
- strokes
- renal artery blockages
- other serious conditions

95
Q

What is Zellweger syndrome?

A

Rare and serious genetic disorder that is linked to peroxisomes
- most severe form of the Zellweger syndrome spectrum
- failure to assemble functional peroxisomes

96
Q

What are some of the symptoms of Zellweger syndrome?

A
  • cause a range of abnormalities in the liver, kidney, muscle, CNS, and other organs
  • associated with the accumulation of very long chain fatty acids (VLCFA) & branched chain fatty acids (BCFA), which are normally degraded in peroxisomes
97
Q

How is Zellweger syndrome linked to peroxisomes?

A
  • because it is caused by a failure to assemble functional peroxisomes
  • which are organelles that play a key role in the metabolism of lipids & other molecules in the body
  • the absence of functional peroxisomes leads to the accumulation of certain fatty acids that are normally degraded in these organelles

BIOS4007 - Bioenergetics and Primary Metabolism (6 decks)

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