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Metabolism > Fatty acid metabolism > Flashcards

Fatty acid metabolism Flashcards

1
Q

What is the maximum total ATP yield of palmitate?

A

104

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2
Q

What are four key groups of lipid?

A

Non-esterified free fatty acids (NEFA)
Sterols such as cholesterol
Triglycerides (TAG)
Phospholipids

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3
Q

What are 4 key functions of lipids?

A

1) Energy source (NEFA and TAG)
2) Structural role in the membrane (PL and cholesterol)
3) Protection (TAG) in adipose stores
4) Signalling roles (PL, steroid hormones, prostaglandins)

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4
Q

What are two ways in which we receive lipids?

A

‘De Novo’ synthesis

Dietary supply

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5
Q

What affect does insulin have on FA metabolism?

A

Secreted in fed state, leads to storage of fat as TAG

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6
Q

What affect do glucagon and adrenaline have on FA metabolism?

A

Secreted in the fasted state, glucagon acts on liver to promote release of FA. Adrenaline promotes ATP production and accelerates metabolism

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7
Q

What is the role of bile in fat digestion?

A

Fat enters the intestine as large triglyceride droplets

Bile salts are released into the intestinal space, they saponify the fats and emulsification them into smaller droplets, thus, increases surface area so lipases have greater action (larger surface area to volume ratio).

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8
Q

Why are do triglyceride droplets need to be treated with bile before digestion?

A

They are large and hydrophobic so inaccessible to digestive enzymes

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9
Q

What enzymes act on small lipid droplets in the small intestine, what do they do?

A

Pancreatic lipases act on the small droplets.

Digest TAG producing NEFA and glycerol.

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10
Q

What is produced after small lipid droplets are treated with lipase, why can they be absorbed by the intestinal cells?

A

Mixed micelles that have a hydrophobic centre and hydrophilic surface, thus can be absorbed by intestinal cells.

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11
Q

What is produced in the ER of absorptive small intestine cells?

A

Chylomicrons

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12
Q

What are the name of small intestine absorptive cells, how are they adapted to function?

A

Enterocytes

Villi, lined with the microvilli of the brush border, provide a lot of surface area for absorption.

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13
Q

How is a micelle changed to a chylomicron?

A

Micelles are absorbed,
digested fatty acids are build up again into TAG, these are combined with cholesterol and phospholipids - forming chylomicrons

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14
Q

Where do newly formed chylomicrons move, what do they join, thus what do they become?

A

Secreted through the basolateral membrane into the lacteals, where they join lymph to become chyle

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15
Q

What is the role of chylomicrons?

A

Transport lipids absorbed from the intestine to adipose, cardiac, and skeletal muscle tissue.

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16
Q

What happens to chylomicrons at their target tissue?

A

Triglyceride components are hydrolyzed by the activity of the lipoprotein lipase, allowing the released free fatty acids to be absorbed by the tissues.

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17
Q

Where is lipoprotein lipase situated?

A

Sits on the surface of target endothelial cells (on the glycocalyx).

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18
Q

What does lipoprotein lipase do?

A

Hydrolyses TAG in the chylomicron into NEFA, this releases NEFA for uptake by adipose and muscle.

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19
Q

What upregulates LPL?

A

Insulin

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20
Q

What happens to absorbed NEFA in fed state in adipose tissue?

A

Resynthesised to triglyceride, NEFA stored as TAG in the tissue.

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21
Q

What happens to fat in adipose tissue in the fasted state?

A

TAG broken down into NEFA for release.

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22
Q

What regulates lipolysis in adipose tissue?

A

Hormone sensitive lipase

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23
Q

What inactivates HSL, what does it do in its inactive form?

A

Insulin activates protein phosphatase ( removes pi from HSL inactivating it)

Stops conversion of TAG to NEFA

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24
Q

What activates HSL, what does it do in its active form?

A

Adrenaline activates PKA through the Gs protein cascade. PKA phosphorylates HSL and thus activates it.

Converts TAG to NEFA

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25
Q

What is the normal plasma NEFA range in fed and fasted state?

A

Fed - 0.3-0.6 mmol/L

Fasted - 0.5-2.0 mmol/L

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26
Q

Why dont all tissues have large TAG stores like adipose?

A

Prevent compromising cell function.

Large amounts of TAG in non-adipose tissue results in steatosis such as fatty liver disease and cardiac lipotoxicity.

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27
Q

What % of ATP in heart comes from FA supplied as NEFA or chylomicron/VLDL complexes?

A

60-70%

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28
Q

Why does the heart use FA for ATP?

A

Most ATP dependent organ so uses FA as energy rich

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29
Q

Does the heart have intracellular TAG stores?

A

Yes

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30
Q

Which organs rely heavily on FA metabolism?

A

Renal cortex, heart, skeletal muscle (type I slow twitch)

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31
Q

What are the differences in metabolism of slow and fast twitch skeletal muscle?

A

Slow twitch: oxidative fibres used more in aerobic exercise. High TAG stores and FA oxidation, many mitochondria.

Fast twitch: glycolytic fibres used more in anaerobic exercise (sprinters). Low TAG stores and FA oxidation, more glycolysis and glycogen stores.

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32
Q

In exercise duration, where does the fuel come from?

A

At rest all energy for skeletal muscle is from plasma NEFA.

In short exercise (<40mins) around 2/3 comes from plasma glucose and intracellular glycogen.

In endurance exercise (>4hours), 2/3 comes from FA and barely any from glycogen (as used up).

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33
Q

What are the overall steps of FA being used to produce ATP?

A

Fat enters cell membrane

Fat is activated (addition of CoA)

Fatty acyl-CoA corsses the mitochondrial inner membrane

Fatty acyl CoA is converted to acetyl CoA in FA oxidation

Acetyl CoA can enter the TCA cycle.

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34
Q

How do FA cross the cell membrane of target organs, what is the main transporter?

A

By either diffusion via flip/flop mechanism or by transporter mediated uptake (allowing more control).

The main transporter is called fatty acid translocase (FAT/CD36).

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35
Q

What does FA bind to inside the cell?

A

Cytoplasmic fatty acid binding protein (cFABP)

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36
Q

How is FA converted to fatty acyl CoA?

A

Addition of co-enzyme A. This is catalysed by acyl-CoA synthetase (ACS). It becomes fatty acyl-CoA.

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37
Q

What is the determining step of NEFA conversion?

A

Addition of co-enzyme A, must be stored or oxidised.

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38
Q

Are there transporters for fatty acyl CoA across the mitochondrial inner membrane?

A

No

39
Q

How does fatty acyl CoA cross the MIM?

A

Carnitine shuttle

40
Q

What conjugates with fatty acyl CoA to allow it to cross the MIM? What enzyme catalyses this conversion?

A

Carnitine (fatty acyl carnitine produced)

CPT1 (carnitine palmitoyl transferase 1)

41
Q

What enzyme de-conjugates fatty acyl CoA with carnitine?

A

CPT2

42
Q

What transporter can move fatty acyl carnitine across the MIM?

A

Carnitine acyl translocase (CAT)

43
Q

Why is the beta oxidation cycle described as a cycle?

A

Each time fatty acyl CoA passes through, it becomes a fatty acyl CoA with 2C shorter than before, until eventually there is no fatty tail left.

44
Q

What about beta oxidation explains why FA are an energy dense fuel?

A

Many FADH2/NADH produced

45
Q

What are the stages of the fatty acid oxidation cycle?

A

Oxidation
Hydration
Oxidation
Thiolysis

46
Q

Which stage produces FADH2?

A

Fatty acyl CoA –> Trans enoyl CoA (oxidation)

47
Q

Which stage produces NADH?

A

Hydroxyacyl CoA –> Ketoacyl CoA (oxidation)

48
Q

What is produced from Beta oxidation (palmitate example)?

A

8 acetyl CoA units (each with 2 carbons)

7 NADH

7 FADH2

49
Q

What different isoforms of the enzyme acyl CoA dehydrogenase are there?

A 
Very long chain (VLCAD)
Long Chain (LCAD)
Medium Chain (MCAD)
Short Chain (SCAD)
50
Q

How is the carnitine shuttle regulated?

A

Malonyl-CoA (intermediate in de novo synthesis) is an allosteric inhibitor of CPT1, preventing futile cycling

51
Q

How do unsaturated FA undergo oxidation?

A

Isomerase coverts cis to trans double bond

Reductase makes it a substrate for ongoing oxidation

52
Q

How FA with odd number of carbons undergo oxidation?

A

Last round starts with 5C

Last cycle generates 1 Acetyl CoA (2 carbons) and 1 PropionylCoA (3 carbons)

PropionylCoA can then be metabolised to SuccinylCoA, to enter the Krebs cycle.

53
Q

How can short chain fatty acids cross MIM?

A

Less than 6 carbons, enter mitochondria directly, bypassing carnitine shuttle.

54
Q

How can very long chain fatty acids undergo oxidation?

A

Must first be shortened in the peroxisomes to 16-18 carbons (peroxisomal β-oxidation) .

Then transferred to mitochondria for β-oxidation.

55
Q

How can branched chain fatty acids undergo oxidation?

A

Starts in peroxisomes with α-oxidation, before transfer to mitochondria for β-oxidation.

56
Q

What does peroxisomal beta oxidation produce?

A

In contrast to mitochondrial β-oxidation, reactions in peroxisome don’t generate ATP. They do generate hydrogen peroxide (H2O2).

57
Q

What is systemic carnitine deficiency, three main symptoms?

A

Genetic disorder, cannot metabolise FA.

Presents with cardiomyopathy as fatty acids are a key fuel source of cardiomyocytes.

Organs have fatty infiltration as fatty acids cant be used in mitochondria so they are stored in tissue.

Often severely hypoglycaemic as glucose is used when fats are deficient.

58
Q

What is ‘de novo’ synthesis?

A

Converts excess carbohydrate/protein for storage in lipid form, generated as FA then converted to TAGs for storage.

59
Q

Where does FA synthesis occur?

A

Cytosol of liver cells

60
Q

Is fatty acid biosynthesis the reverse of fatty acid oxidation?

A

Chemically the reverse of fatty acid oxidation but mechanistically different processes.

61
Q

What is the initial stage of FA biosynthesis?

A

Elongation of acetyl CoA to a 3 carbon unit called malonyl CoA.

Reaction of Acetyl CoA with a bicarbonate ion.

Catalysed by acetyl-CoA carboxylase and requires one molecule of ATP.

62
Q

What is malonyl CoA and acetyl CoA coupled with before they enter the biosynthesis pathway, what enzyme adds this?

A

ACP (acyl carrier protein)

Transacylase enzyme

63
Q

What reductant is used for FA biosynthesis?

A

NADPH

64
Q

What is the final product of FA biosynthesis (example)?

A

Passes 7x to produce palmitoyl-ACP

65
Q

How is palmitoyl-ACP converted to palmitate FA?

A

Hydration via palmitoyl thioesterase

66
Q

What is unique about the enzymes in biosynthesis compared to oxidation?

A

Enzymes joined in a single polypeptide chain (fatty acid synthase

67
Q

How are odd chain length FA synthesised?

A

Introduction of propionyl-ACP rather than acetyl-ACP

68
Q

Where are the enzymes that promote longer chain FA biosynthesis found?

A

Produced by enzymes on the cytoplasmic face of the smooth endoplasmic reticulum

69
Q

How are unsaturated FA produced?

A

ER systems introduce double bonds to long chain FA

70
Q

What are essential FA and why are they essential?

A

Mammals lack the enzyme to introduce double bonds beyond C-9

SO linoleate (18:2 cis-D9,D12) and linolenate(18:3 cis-D9,D12,D15) are considered “essential” fatty acids.

71
Q

What is the action of domain I of FAS, what enzymes make it up?

A

The substrate entry domain containing.

MAT: the malonyl/ acetyl transacylases

KS: the ketoacyl-ACP synthase (the condensing enzyme)

DH: the dehydratase

72
Q

What is the action of domain II of FAS, what enzymes make it up?

A

The reduction unit containing.

ER: the enol-ACP reductase

KR: the ketoacyl-ACP reductase

ACP: the acyl carrier protein

73
Q

What is the action of domain III of FAS, what enzymes make it up?

A

The palmitate release unit containing

TE: the thioesterase

74
Q

How can pyruvate (carbohydrates) be converted to fatty acids?

A

Converted to acetyl CoA in the mitochondria, which then enters the biosynthetic pathway

75
Q

How can acetyl CoA produced from pyruvate in the mitochondria move to the cytosol for fatty acid biosynthesis? Describe the process?

A

Citrate shuttle

Citrate (produced by the condensation of acetyl CoA with oxaloacetate) is carried across the inner mitochondrial membrane into the cytosol.

There it is cleaved by ATP citrate lyase into acetyl-CoA and oxaloacetate.

The cytosolic acetyl-CoA is carboxylated by acetyl CoA carboxylase into malonyl CoA, the first committed step in the synthesis of

76
Q

What can happen to the cytosolic oxaloacetate moved via citrate shuttle?

A

The oxaloacetate can be used for gluconeogenesis (in the liver), or it can be returned into mitochondrion as malate.

77
Q

Where is the main site of regulation for FAS?

A

Acetyl-CoA carboxylase

78
Q

What allosterically activates and inhibits acetyl-CoA carboxylase?

A

Citrate allosterically activates

Long chain fatty acyl CoA allosterically inhibits

79
Q

What covalently activates/inhibits acetyl-CoA carboxylase?

A

Inactive when phosphorylated

AMP-activated protein kinase activated by elevated levels of AMP, thus when in a low energy state fatty acids will not be synthesised, they will be used for energy.

Glucagon activates PKA inactivating enzyme.

Insulin activates protein phosphatase 1 which activates the enzyme by dephosphorylating it

80
Q

What process converts fatty acyl CoA to TAG?

A

Esterification

81
Q

How are TAGs made in the liver transported to tissue for storage and use?

A

In VLDLs

82
Q

Dietary fatty acids are packaged by the liver into very low density lipoproteins for distribution to the rest of the body.

A

False, de novo FA are

83
Q

What state does FA biosynthesis occur in?

A

Fed state, when fasting they will be used for energy

84
Q

In the synthesis of triglyceride from Acetyl CoA, a key intermediate that is produced is…

A

Malonyl CoA

85
Q

Acetyl CoA is transported out of the mitochondrial matrix to the cytoplasm for fatty acid biosynthesis in the form of …

A

Citrate

86
Q

What is activated after a meal…

A

Fatty acid biosynthesis

87
Q

Malonyl CoA blocks uptake of fatty acids into the mitochondrion for oxidation by inhibiting …

A

CPT1

88
Q

What is CPT1 also called?

A

Fatty acyl carnitine transferase

89
Q

In the fed state what is the preferred energy source for the heart?

A

Exogenous fatty acids

90
Q

The enzyme responsible for the release of fatty acids from the VLDL particle is?

A

Lipoprotein lipase

91
Q

A key intermediate in the biosynthesis of fatty acids…

A

Malonyl CoA

92
Q

Each cycle of oxidation what is produced?

A

1 Acetyl CoA (2C)
1 NADH
1 FADH2

93
Q

What does biosynthesis require for each cycle?

A

2 NADPH

Metabolism (13 decks)

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