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Nutrition & Metabolism > W5 - Fat Metabolism > Flashcards

W5 - Fat Metabolism Flashcards

1
Q

What are fats usually carried in around the body because they have detergent like properties?

A

lipoproteins

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2
Q

What are simple lipids

A

Lipids composed of only FAs, glycerols + alcohols

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3
Q

What are complex lipids

A

Lipids that contain FAs, glycerols + other groups

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4
Q

What do lipoproteins carry?

A

TAGs

Cholesterol

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5
Q

Which parts of a lipoprotein are hydrophilic + which are hydrophobic?

A

Hydrophilic shell

Hydrophobic core

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6
Q

What does the outer layer of a lipoprotein contain?

A

Monophospholipids

Cholesterol

Protein

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7
Q

There are 4 main lipoproteins in the human body.

What do they carry?

A

2 are main carries of TAG

2 of cholesterol esters

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8
Q

List the 4 main lipoproteins

A

Chylomicrons

VLDL (Very low density lipoproteins)

LDL

HDL

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9
Q

HDL or LDL for chylomicrons

A

ULDL (ultaLDL)

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10
Q

Which is the biggest lipoprotein?

A

Chylomicrons

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11
Q

What does the chylomicron carry?

A

90% TAG

Some Cholesterol esters (CE)

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12
Q

% of protein + lipids in chylomicrons

High or low?

A

Protein = lowest %

Lipids = highest %

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13
Q

Where are chylomicrons made?

A

Small intestine

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14
Q

What do VLDLs carry?

A

TAG

Cholesterol esters

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15
Q

Where are VLDLs made?

A

Liver

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16
Q

What do LDLs carry?

A

ONLY cholesterol esters

LDLs - considered bad cholesterol

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17
Q

What do HDLs carry?

A

ONLY cholesterol esters

HDLs - considered good cholesterol

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18
Q

Which lipoprotein has the highest % of protein?

A

HDL

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19
Q

What are probably the strongest lipid predictor for CV disease?

A

HDLs

Higher content in blood = ⬇️ risk of CV disease

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20
Q

Quick overview of the consumption + absorption of fats

A

TAGs broken down by lipase

Packaged into myocells

Transferred into epithelial

Synthesised by chylomicrons

Into lacteal which drains into lymph, then blood + subclavian vein.

== Chylomicrons in circulation

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21
Q

Fat absorption has happened in the postprandial state.

Want to store the fat.

Where do the chylomicrons travel to?

Then what happens?

A

Extra hepatic tissues

Bv here have LPL on their walls.

= Chylomicrons dock onto this enzyme to be broken so the TAGs can be broken down to release FAs + glycerol.

FAs enter tissues.

Repackaged into TAGs + stored.

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22
Q

What is the chylomicron called once it has lost most of its TAGs when docked onto the lipoprotein lipase in bv walls?

A

Chylomicron/lipoprotein remnant

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23
Q

Where is the Chylomicron/lipoprotein remnant transported to

A

Liver

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24
Q

What happens to the Chylomicron/lipoprotein remnant in the liver?

A

Broken down + reutilised.

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25
Q

What happens to the cholesterol of the Chylomicron/lipoprotein remnant once it has been broken down + reutilised in the liver?

A

Joins a pool of cholesterol in the liver where has many functions.

1 of which = Bile created

Can also be packaged into LDL to take cholesterol to the other bodys tissues.

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26
Q

How can more cholesterol enter bloodstream?

A

Low HDL levels

High LDL

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27
Q

What does the liver do with the fat it contains?

A

Packages it into VLDL

VLDL sent to peripheral tissues so they can store the TAG.

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28
Q

What are the 4 ways of regulating FA utilisation?

A

Lipolysis of TAG to form FFAs

Re-esterification of FAs or mobilisation from adipose tissue

Transport of ACoA into mit

Availability of FAD + NAD for b-oxidation

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29
Q

In what states can adipocytes in adipose tissue be used?

A

Post absorptive states + exercise

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30
Q

How is HSL (hormone sensitive lipase) regulated?

A

By phosphorylation.

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31
Q

What enzyme converts the inactive form of HSL to its active form and how?

A

Protein kinase

By adding a phosphate group.

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32
Q

What stimulates protein kinase to convert inactive HSL to active HSL?

A

Ca2+

Adrenaline

= Both i.e from exercise

Growth hormone cortisol (i.e from stress)

33
Q

When wouldn’t you want HSL in its active form?

A

Just after eating

34
Q

Enzyme to convert HSL in its active form to HSL in its inactive form?

A

Phosphatase

35
Q

What stimulates phosphatase to convert HSL in its active form to HSL in its inactive form?

A

Insulin

36
Q

Why is it difficult to get FAs out of the adipocytes?

A

Due to re-esterification

37
Q

Does the glycerol in the adipocyte need to go or can it stay?

A

Needs to go.

Can’t be reused to make TAG.

38
Q

How is a fatty acyl-CoA converted back into TG?

A

By reesterification + the addition of a-glycerol-P

39
Q

What happens to lipolysis with exercise?

A

⬆️

40
Q

What is FA transport across cell membranes dependent on?

A

Plasma FA conc

41
Q

What are the functional protein carriers allowing FA transport across cell membranes?

A

FABP (FA binding protein)

FAT/CD36 (FA translocase)

FATP (FA transport protein)

42
Q

What happens to the FA once inside the cell?

A

Becomes fatty-acyl-CoA by Acyl-CoA synthethase enzymes.

43
Q

Where can the FAs come from when moving from the blood into the interstitial fluid?

A

Chylomicron

VLDL

Albumin

44
Q

How do FAs move from the interstitial fluid into the sarcoplasm of a muscle cell?

A

⬇️ conc grad through FAT/CD36.

45
Q

What happens to the Fatty-acyl-CoAs in the cell?

A

Can either:

  • be incorporated into lipid pools

OR

  • be oxidised by mit for energy
46
Q

Give an example of a lipid pool in muscles

A

IMTG droplets

Intramuscular TG

47
Q

Lipolysis of IMTG, by what enzyme?

A

Active form of HSL

48
Q

What is protein kinase stimulated when converting inactive form of HSL to active form for the lipolysis of IMTG?

A

Ca2+

Adrenaline

AMP

49
Q

Membranes of the mitochondria in regards to lipid permeability

A

Outer - permeable to lipids

Inner - IMpermerable to lipids

50
Q

Where is the CPT 1 located in the mitochondria?

A

Outer membrane

51
Q

What does CPT 1 do in the carnitine shuttle?

A

Attaches carnitine group to acyl-CoA

removes CoA from acyl-CoA

== Acyl-carnitine

52
Q

What in the mitochondria helps acyl-carnitine move across the inner membrane into the mit matrix?

A

CACT (Carnitine acyl carnitine translocase)

53
Q

What must happen once the acyl-carnitine has entered the mit matrix?

How does this happen?

A

Need to remove carnitine group

Put CoA back on

== By CPT2

=== AcylCoA now ready in mitochondrial matrix

54
Q

What happens to the AcylCoA once in the mit matrix?

A

Undergoes b-oxidation

55
Q

What are the later forms of Acyl CoA as it goes through the b-oxidation cycle in the matrix of the mitochondria before entering the TCA cycle as Acetyl-CoA (ACoA)?

A

Acyl CoA

2-trans-enoyl CoA

L-3-hydroxyl acyl CoA

3-ketoacyl coA

56
Q

Which is the rate limiting enzyme in the b-oxidation cycle in the matrix of the mitochondria for Acyl-CoA

A

3rd enzyme = Beta hydroxy Acyl CoA dehydrogenase (beta HAD)

57
Q

What happens to plasma FA conc during prolonged exercise?

A

⬆️ after an initial drop

58
Q

Why is there an initial drop in plasma FA during prolonged exercise when looking at a graph?

A

Slow FA mobilisation from adipose tissue

Uptake of FA from working muscles straight away

59
Q

Why does plasma FA conc increase during prolonged exercise?

A

Insulin is red. so less glucose in blood

Adrenaline is increased.

Glycerol stores may be depleted.

== ⬆️ HSL = ⬆️ lipolysis = ⬆️ FA in blood

60
Q

What does increase FA in plasma result in during exercise?

A

Greater flux = drives a FA oxidation increase

61
Q

What does an increased FA flux into plasma do to CHO?

A

⬆️ acetyl-CoA = inhibits PDH + PFK, ⬆️ citrate accumulation

== G-6-P accumulates = glycogenolysis inhibited = ⬇️ con grad for glucose uptake

== ⬇️ CHO oxidation

62
Q

Which of LDL + HDL has a longer half-life ?

A

LDL

Lasts 1.5-2 days

63
Q

How long do chylomicrons VLDLs last in the body?

A

Few hours

64
Q

What does damage to the LDL enable?

A

⬆️ its affinity to bind to a receptor on macrophages.

Taken into macrophage,

65
Q

How can LDLs be damaged?

A

Toxins

Free radicals

High glucose

66
Q

Do macrophages have cholesterol sensors?

A

No

67
Q

What does it mean that macrophages don’t have cholesterol sensors?

A

They keep taking in LDLs

== Changed into a foam cell (bigger than a macrophage)

68
Q

Can foam cells penetrate bv walls?

A

yes

69
Q

What can an accumulation of foam cells on vessel walls cause?

A

Inflammation which can lead to fatty streaks. –> Atherosclerosis

70
Q

What can HDL do in regards to the foam cells?

A

Can dock onto its receptor + remove the excess cholesterol.

Takes cholesterol to liver where used for bile acids

71
Q

Monounsaturated fats have how many double bonds

A

1

72
Q

After FAs have been released from fat cells, what is the name of the protein carrier that transports them in blood?

A

Albumin

73
Q

What is lipolysis NOT stimulated by?

A

Insulin

74
Q

How are long chain fatty acids transported from the small intestine through the body?

A

In chylomicrons

75
Q

Transport of fatty acids across the inner mitochondrial membrane is dependent upon…

A

Carnitine

76
Q

What is involved in the transport of short chain fatty acids around the blood

A

Albumin

77
Q

Increased glycogenolysis in exercise is likely due to…

A

Increased AMP

78
Q

What will inhibition of PFK do to CHO oxidation + glycolysis?

A

Inhibits it

79
Q

What effect will a reduction in FAD have on flux through beta oxidation?

A

Reduce it

Nutrition & Metabolism (17 decks)

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