W3 - Fat metabolism Flashcards

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1
Q

What is LDL associated with?

A

⬆️ risk of heart disease

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2
Q

What are each ends of the FA called?

A

Omega

Carboxyl

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3
Q

How might adipose tissue turnover decline?

A

If health status declines

i.e athletes have a very high turnover rate

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4
Q

What cytokines does adipose tissue secrete?

A

Inflammatory cytokines

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5
Q

When are lipids insoluble?

A

In aqueous solutions

i.e blood

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6
Q

How is fat transported in the blood?

A

In chylomicrons or lipoproteins

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7
Q

FAs oxidised in the mitochondria of skeletal muscle during exercise are derived from 2 main sources. What are these?

A

Adipose tissue

Muscle TAG (delivered in chylomicrons + VLDL).

(Plasma TAG may also be used).

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8
Q

TAG in adipose tissue is split into FA + glycerol. What happens to these?

A

Glycerol is released into circulation w/ some of the FAs,

Small & of FAs are NOT released into circulation but used to form new TAF in the adipose tissue = Reesterification.

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9
Q

What happens to the FAs that have been released from adipose tissue?

A

Transported to other tissues + can be uptake by skeletal muscle during exercise.

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10
Q

What happens to the glycerol released from the adipose tissue?

A

Transported to liver

  • Acts as a gluconeogenic substrate to form glucose.
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11
Q

What can circulating TAG i.e VLDL do temporarily?

A

Bind to LPL to allow FAs to be split off so that they can be taken up by muscle.

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12
Q

What are IMTG split by?

A

HSL

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13
Q

What are the steps that could limit fat oxidation

A

Lipolysis

Removal of FA from fat cell

Transport of fat by bloodstream

Transport of FAs into muscle cell

Transport of FAs into mitochondria

Oxidation of FAs in b-oxidation pathway + TCA cycle

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14
Q

Where are most FAs stores as?

A

TAG in subcutaneous adipose tissue.

These must be mobilised + transported to the site of oxidation.

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15
Q

What do adipocytes contain?

A

Lipases that breaks down TAG

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16
Q

What does the SNN stimulate HSL to do?

A

Split TAG into FAs + glycerol.

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17
Q

What does the conversion of the inactive form of HSL to the active form depend on?

A

SNN + circulating epinephrine.

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18
Q

Where is norepinephrine release from in the SNN?

A

It’s nerve endings

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19
Q

What is often used as a measure of lipolysis?

A

Measurement of glycerol in the blood

20
Q

What % of FAs are reesterified in lipolysis at rest?

A

~70%

21
Q

What happens to reesterification during exercise?

A

Suppressed to incr availability of FAs in adipocyte.

22
Q

What stimulates lipolysis during exercise?

A

Catecholamines released from the adrenal gland

23
Q

What does reesterification depend on?

A

Rate at which FA are removed from the adipocyte by the blood

Rate of G-3-P prod

Activity of TAG synthesising enzymes

24
Q

What does the removal of FAs from adipocyte into the bloodstream depend on?

A

Blood flow to adipose tissue

Albumin conc in blood

No. of free binding sites for FAs on albumin

25
Q

What is the most abundant protein in plasma?

A

Albumin

  • Acts as a carrier protein transporting FAs
26
Q

What happens when albumin arrives at target tissue?

A

Binds to specific ABPs

Binding to this aids the release of FAs from albumin + their uptake.

27
Q

What does LPL in the vascular wall do?

A

Hydrolyses some TAG in circulating lipoproteins passing through the capillary bed.

== FA are released, muscle takes them up to use for oxidation.

28
Q

FA uptake from plasma lipoprotein TAG

A

Happens slowly

Accounts for less than 3% of the energy expenditure during prolonged exercise.

29
Q

What transport proteins are found in the sarcolemma/

A

FABPpm protein

FAT/CD36 protein

30
Q

What does muscle contraction do to plasma membrane FAT/CD36?

A

Increases it = incr. FA transport into cells.

31
Q

What are FAs bound to in the sarcoplasm?

A

FA-binding protein (FABPc).

– Thought to be responsible for the transport of FAs from sarcolemma to mitochondria.

32
Q

Which muscle fibres have a higher content of IMTG?

A

Type 1

33
Q

Muscle contains HSL

What is it activated by

A

b-adrenergic stimulation

34
Q

Muscle contains HSL

What is it inhibited by

A

Insulin

35
Q

What can happen with the FAs liberated from IMTG?

A

Can be released into blood

Reesterified

Oxidised w/in muscle

36
Q

What are FAs bound to until transported into mitochondria?

A

FABPc

37
Q

What can FAs in the cytoplasm be activated by?

A

ACoA synthetase or thiokinase

38
Q

What is formed once the ACoA synthetase or thiokinase meets with the FAs in the cytoplasm?

A

Forms ACoA complex

39
Q

FAs in cytoplasm can be activated by ACoA synthetase or thiokinase to form ACoA complex.

What happens next with this complex?

A

Used for synthesis of IMTGs

OR

Is bound to carnitine under the influence of the CPT1 enzyme.

40
Q

What is the 1st step in transport of FA into the mitochondria?

A

Bonding of carnitine + activated FA

41
Q

What is released when carnitine binds to FA?

A

CoA

42
Q

CHO + fat are always oxidised as a mixture

What does the prominent fuel used depend on?

A

Intensity

Duration

Level of aerobic fitness

Diet

CHO intake before or during exercise

43
Q

What does the rate of lipolysis in adipose tissue depend on?

A

Circulating conc of hormones (epinephrine stimulates lipolysis + insulin inhibits lipolysis).

44
Q

When does fat oxidation peak ?

A

~50-60% vo2 max

45
Q

What does training do to fat oxidation?

A

Enhances

46
Q

What are the adaptations contributing to stimulation of fat oxidation in trained athletes?

A

⬆️ mit density + ⬆️ no, of oxidative enzymes in trained muscle

⬆️ capillary density = enhances FA delivery to muscle

⬆️ FABP conc which may facilitate uptake of FAs across sarcolemma

⬆️ CPT conc which facilitates transport of FAs into mitochondria