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Bioenergetics > Week 9 - Lipid Metabolism > Flashcards

Week 9 - Lipid Metabolism Flashcards

1
Q

What are the ways in which lipids are categorised?

A

FA

Triacylglycerols

PL

Sterols

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2
Q

Are lipids hydrophobic or hydrophilic?

A

Hydrophobic

But some are amphiphatic

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3
Q

Describe carboxylic acids

A

Contain long alkyl chain w/ a carboxylic-acid group at 1 end.

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4
Q

How many C atoms do the majority of fatty acids contain

A

16

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5
Q

How many C atoms do short chain FA generally have

A

4-6 C

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6
Q

How many C atoms do medium chain FA generally have

A

8-12 C

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7
Q

How many C atoms do long chain FA generally have

A

14 or + C

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8
Q

Double C bonds in sat + unsat FA

A

Sat = NO C=C bonds

Unsat = 1 or more C=C bonds

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9
Q

What does the 1st no. of a FA represent?

i.e linoleum acid 18:2 (9,12)

A

No. of C atoms in FA

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10
Q

What does the 2nd no. of a FA represent?

i.e linoleum acid 18:2 (9,12)

A

No. of double bonds

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11
Q

What is the configuration of double bonds in naturally occurring FA?

A

Almost always cis

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12
Q

How are unsat FA ID

A

By the position of the double bond closest to the methyl group

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13
Q

How are trans double bonds introduced?

A

Manufacturing process

– Unsat FAs are hydrogenated to make them more solid.

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14
Q

What are the 3 most common FAs

A

Palmitic acid

Oleic acid

Stearic acid

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15
Q

What is palmitic acid called at a pH of 7

A

Palmitate

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16
Q

What are the FAs that humans can’t make

A

Linoleic acid

𝛼-linolenic acid.

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17
Q

Why are TAGs insoluble in H20

A

Due to large degree of hydrophobic hydrocarbon components.

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18
Q

How many Kcal/g does fat provide

A

9Kcal/g

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19
Q

How many kJ/g does fat provide

A

37kJ/g

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20
Q

How many Kcal does 1kg of adipose tissue provide

A

7000Kcal

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21
Q

Describe glycerol

A

3C mol

w/ 3 alcohol groups

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22
Q

Define an ester

A

Comb. Of an acid + alcohol

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23
Q

What does the physical state of a TAG depend on?

A

Length of C chain

No. of double bonds

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24
Q

What does it mean in regards to melting points if the lengths of the FA chains re short + there’s more double C bonds

A

Lower melting points

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25
Q

Summarise TAG catabolism

A

TAG – (HSL + H20) –> Diacylglycerol – (HSL + H20) –> monoacylglycerol – (H20 + monoglyceride lipase + HSL) –> Glycerol + 1 FA

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26
Q

Are PL diglycerides

A

YES

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27
Q

What is on the 3rd position of a PL

A

Phopshoric acid residue to which 1 of 4 different base groups attaches.

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28
Q

What are the 4 different base groups that can attach to the phosphoric acid on a PL

A

Choline

Inositol

Serine

Ethanolamine

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29
Q

What is the most abundant PL

A

Lecithin

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30
Q

Where are dietary fats mainly digested + by what?

A

Small intestine

By action of bile salts + pancreatic lipase

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31
Q

Briefly describe how the dietary fats are digested

A

Bile salts break large globules of fat –> smaller micelles (making them more accessible to lipase)

Pancreatic lipase converts TG–> monoglycerides, free FA + glycerol.

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32
Q

What is lipolysis

A

Hydrolysis of triacylgycerols (TAG) found in adipose tissue

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33
Q

When is lipolysis favoured?

A

In cond. of:

  • ⬆️ energy need
  • Low calorie dieting
  • Fasting
  • Cold body
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34
Q

What hormones enhance TG breakdown

A

Epinephrine

Norepinephrine

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35
Q

When are epinephrine + norepinephrine released

A

When sympathetic tone ⬆️

i.e during exercise

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36
Q

List other lipolytic hormones

A

Cortisol

Thyroid hormones

Insulin

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37
Q

What is the enzyme req for the hydrolysis of the 1st ester bond in TAG?

A

Adipose TG lipase

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38
Q

What is intramuscular TAG

A

TAG stored in skeletal muscle

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39
Q

What happens to intramuscular TAG when hydrolysed

A

FA generated are oxidised w/ in contracting fibre.

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40
Q

How is glycerol (from lipolysis) catabolised:?

A

Glycerol –> glyceraldehyde 3-phosphate

Then to glucose (if ATP supply in a cell is high = gluconeogenesis)

OR

Enters catabolic pathway to pyruvic acid (If ATP supply is low)

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41
Q

How are FA (from lipolysis) catabolised:?

A

In matrix of mit.

Enzymes remove 2C from long chains + attach it to CoA to form Acetyl-CoA which enters the TCA cycle.

Hepatocytes can take 2 Acetyl-CoA mol at a time + condense them to acetoacetic acid. The CoA is liberated but can’t diffuse out of cells.

Some acetoacetic acid –> β-hydroxybutyric + acetone.

= The formation of these 3 ketone bodies is ketogenesis.

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42
Q

What % of energy from TAG comes from the FAs

A

95%

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43
Q

Are ketone bodies able to leave hepatocytes + enter blood stream?

Why?

A

Yes as they can freely diffuse through plasma membranes

44
Q

What do other cells do after up taking acetoacetic acid

A

Attach its 4C (from acetoacetic acid) to 2 CoA mol to form…

2 Acetyl-CoA mol which can enter the TCA cycle for oxidation.

45
Q

Can hepatocytes use the acetoacetic acid they make for ATP production?
Why?

A

No

As they lack the enzyme that transfers acetoacetic acid back to CoA.

46
Q

Where does lipolysis take place

A

Locations other than in fat cells:

i.e, hydrolysis of dietary TAG in small intestine, by pancreatic lipase.

Hydrolysis of TAG in blood lipoproteins by lipoprotein lipase.

Intramuscular TAG is hydrolysed by a muscle-specific HSL, which generates FAs that are immediately available as a fuel for that fibre.

47
Q

How many Kcal of H20 soluble fuel does the brain req per day?

A

500Kcal

48
Q

Can FA be converted into glucose for the brain(i.e) to use?

A

no

49
Q

Can CHO be converted into FA?

A

yes

50
Q

Can aa be converted into FA?

A

YES

51
Q

Can FA be converted into aa?

A

NO

52
Q

What are the effects of insulin in the blood on muscle?

A

Inhibits muscle lipoprotein lipase = no fat breakdown

53
Q

What are the effects of insulin in the blood on adipose tissue?

A

Stimulates lipoprotein lipase

Inhibits hormone sensitive enzyme lipase to prevent fat from being released into bloodstream.

⬆️ in chylomicrons = ⬆️ TAG, glycerol + FAs go into adipose tissue to be stored.

54
Q

What are the effects of insulin in the blood on the liver?

A

Synthesis of new FAs, TAG + cholesterol

55
Q

What is the feeding state?

A

Storing fat - feeding state

Just eaten.

Incr. blood glucose levels, incr. in lipids.

Stimulation of insulin = incr. insulin in blood which has an effect on 3 diff. organs:

Muscle, adipose tissue + liver

56
Q

What is the fasting state?

A

Using Fat for Energy — Fasting State

Blood glucose levels start to drop, as been time since eating.

= Inhibits secretion of insulin = decr. Insulin in blood.

Glucagon release is stimulated.

57
Q

What are the effects of glucagon in the blood on adipose tissue?

A

inhibits lipoprotein lipase to prevent breakdown of chylomicrons.

But stimulates thehormone sensitive enzyme lipase which breaks down fat —> bloodstream.

58
Q

What are the effects of glucagon in the blood on muscle?

A

Stimulates the muscle lipoprotein lipase

59
Q

What are the 2 pathways

A

Exogenous

Endogenous

60
Q

Exogenous pathway

A

Cholesterol from dietary + biliary sources is absorbed in the intestine + enter circulation as a component of chylomicrons.

61
Q

Endogenous pathway

A

Cholesterol is synth. by the liver + extra hepatic tissues + enters circulation as a component of lipoproteins or is secreted into bile.

62
Q

What are the main lipid transport molecules

A

Chylomicrons

Lipoproteins

Albumin

63
Q

Describe chylomicrons

A

Large lipoprotein particles containing TG packaged w/ cholesterol.

64
Q

Where are chylomicrons synthesised

A

Small intestine

65
Q

What happens once the chylomicrons have left the enterocytes?

A

Enter the lymphatic capillaries

Pass into blood stream

Deliver fats to tissues

66
Q

Examples of lipoproteins

A

HDL

LDL

VLDL

67
Q

What do lipoproteins allow the transport of

A

H20-insoluble fats w/in aqueous env.

68
Q

Where can lipoprotein lipase be found

A

Capillary walls

69
Q

What does lipoprotein lipase do

A

Hydrolyses TG –> FA + glycerol

70
Q

What happens once lipoprotein lipase has hydrolysed TG?

A

FA + glycerol pass through capillary wall to tissues where they’re oxidised for energy or re-esterised for storage.

71
Q

What happens to fats that are synthesised endogenously in the liver?

A

Packaged into another type of lipoprotein = VLDL

To be transported to tissues where TG are extracted in the same way.

72
Q

What happens when FA undergo β-oxidation?

A

Generates Acetyl-CoA.

Each round removes 2C from FA chain.

73
Q

What does albumin transport

A

Un-esterified FA

74
Q

What are the 3 main steps req. for the mobilisation of stored fat + oxidation of FFAA

A

Release of FFAA from TAG

β-oxidation of FFAA —> TCA cycle —> ATP

𝜶- oxidation of FFAA —> TCA cycle

75
Q

Explain the release of FFAA from TAG

A

In order for lipolysis to occur, HSL needs to be activated by epinephrine or glucagon. – Triggering a reaction that req. ATP.

Also activated protein kinase which also req ATP.

TAG breakdown by triglyceride lipase.

76
Q

Fate of glycerol after the release of FFAA from TAG

A

β-oxidation can’t occur in the adipose tissue

Glycerol can’t be phosphorylated due to lacking glycerol kinase.

So, glycerol is transported in blood to liver.

77
Q

Fate of glycerol after the release of FFAA from TAG

What happens once glycerol has been transported to the liver

A

Phosphorylated + converted to GLYCEROL PHOSPHATE then to DIHYDROXYACETONE-PHOSPHATE / DHAP which eventually becomes PYRUVATE.

– All reversible

78
Q

What happens once pyruvate becomes acetyl Co-A

A

Enters β-oxidation + not reversible

79
Q

Fate of FFAA after the release of FFAA from TAG

A

Unesterified FA move through cell membrane of adipocyte.

Bind to albumin in plasma where they’re transported to tissues where FA enter cells, get activated to CoA derivatives + oxidised for energy.

80
Q

Why is it important that 2C fragments are removed from a FA at a time?

A

Allows 1 to calculate how much ATP is yielded from each of the FAs

81
Q

Carnitine Shuttle

A

Allows Acetyl-CoA (hydrophobic) to cross inner mit. membrane from cytosol –> matrix where TCA cycle + β-oxidation occurs

82
Q

What enzyme converts long chain FA to Acetyl CoA

A

CoA synthase / thiokinase

83
Q

Carnitine

A

Mol. key to transporting acyl CoA into mit.

84
Q

How is carnitine from mit. transported to cytosol?

A

By carrier protein translocase

85
Q

What does CAT-1 / carnitine palmitoyltransferase I do in the cytosol

A

Facilitates the addition of an Acyl mol to carnitine + the regeneration of CoA.

Acyl carnitine can be transported into mit again by action of same carrier protein = translocase.

86
Q

What does CAT-2 / carnitine palmytoyltransferase 2 do in the mitochondria

A

Catalyses the reaction of Acyl + CoA –> Acyl CoA + liberates carnitine

87
Q

What size FA can cross the inner mit w/out CARNITINE

A

FA w/ less than 12C

88
Q

When can FA enter the TCA cycle

A

Only if enough oxaloacetate has been generated from pyruvate.

89
Q

Give a summary of the energy yielded from a 16C FA

A

16C broken down in 2s to become 14C, 12C…

FADH2 provides 2 ATP when oxidised w/ the ETC

NADH provides 3.

From a 16C FA = 14ATP from FADH2, 21 ATP from NADH + from the TCA cycle 96 in total == 131 ATP.

90
Q

𝜶- oxidation

A

When there’s branched chain FA as they’re not substrates for Acetyl CoA dehydrogenase due to the methyl group present.

= Instead, branched chain FA are hydroxylated at the 𝜶-carbon by FA 𝜶-hydroxylase. — Product is decarboxylated + then activated to it CoA - a substrate for enzymes of β-oxidation.

91
Q

Ketone bodies

A

H20 soluble, energy-rich compounds that are easily transported across cell membranes.

92
Q

Give examples of ketone bodies

A

acetoacetate

β-Hyroxybutyrate

acetone

93
Q

What are the special circumstances under which ketone bodies are only formed under?

A

Glucose deficiency i.e due to fasting or diabetes mellitus.

In this case, to supply extrahepatic tissues that can’t breakdown FA, the liver switches to gluconeogenesis + the breakdown of FA. — For this breakdown, β-oxidation splits FA in liver into acetyl CoA. Usually, the Acetyl CoA is further metabolised in the TCA cycle. But conversion of Acetyl CoA —> ketone bodies in ketogenesis ONLY starts when there’s a deficiency of oxaloacetate as well as low glucose.

94
Q

What happens in diabetes mellitus

A

Cellular glucose uptake is inhibited, causing intracellular glucose deficiency

95
Q

Liver doesn’t use ketone bodies for its own energy supply, so what does it do with them?

A

Releases them into the blood for cells of the brain, skeletal + cardiac muscle cells.

96
Q

What happens after ketone bodies have been released into the blood

A

They reach the extra hepatic tissues which absorb + convert them back into 2 mol of Acetyl CoA in ketogenolysis.

97
Q

What happens with the 2 mol of Acetyl CoA after ketogenolysis in the extra hepatic tissues?

A

Enter TCA cycle as there’s no oxaloacetate deficiency in the extra hepatic tissues so Acetyl CoA can contribute to the generation of ATP in the cells.

98
Q

Why might there be a deficiency of oxaloacetate

A

Low glucose levels inhibit glycolysis so almost no pyruvate available to form oxaloacetate

FA degradation = accumulation of Acetyl CoA meaning amount of acetyl CoA is far more than the amount of oxaloacetate available to TCA cycle.

99
Q

Describe the ketogenic diet

A

Very low CHO

High fat

Triggers the metabolic fasting state of the body

100
Q

What happens in the ketogenesis process

A

Ketone bodies are formed from Acetyl CoA (arising mainly from breakdown of FA) in mit of hepatocytes.

101
Q

Steps of the ketogenesis process

A

2 mol of Acetyl CoA – (thiolase) –> Acetoacetyl-CoA

3rd mol of Acetyl CoA is used to convert Acetoacetyl-CoA –(HMG-CoA synthase)–> HMG-CoA

HMG-CoA – (HMG-CoA lyase) –> Acetoacetate (ketone body). – Acetyl CoA is cleaved from mol.

== To yield 1 mol of acetoacetate, 2 mol. of Acetyl CoA are needed.

Acetoacetate – (β-Hyroxybutyrate dehydrogenase)—> β-Hyroxybutyrate (by being reduced).

102
Q

What os the ketogenolysis process

A

Ketone bodies are converted back into acetyl-CoA which is fed into TCA cycle + used for ATP synth.

103
Q

Steps in the ketogenolysis process

A

Acetoacetate – (thiophorase)–> Acetoacetyl-CoA

Thiolase catalyses formation of AcetylCoA

104
Q

Is acetone metabolised?

A

no

105
Q

What happens instead with acetone as it isn’t metabolised

A

Excreted as a metabolic end product in exhaled air.

106
Q

Ketoacidosis

A

In type 1 diabetes mellitus

Serum pH below 7.3 — Drop is caused by acetoacetate + β-Hyroxybutyrate as they both have an acid group that cleaves its proton under physiological cond.

High levels of ketone bodies in blood + urine.

Bioenergetics (12 decks)

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