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Y1 Nutrition & metabolism > Fat metabolism > Flashcards

Fat metabolism Flashcards

1
Q

What are fats

A
  • Long carbon chains (length varies) with different degrees of saturation
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2
Q

More saturation = ?

A

More energy because there are more double bonds so less oxygen (making them energy dense) meaning more oxygen need for oxidisation

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3
Q

What is fat stored as?

A

Triacylglycerol (3 Fatty acids and glycerol backbone)

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4
Q

Why is cholesterol important? (3)

A
  • membrane stability
  • steroid hormone synthesis
  • Vitamin D synthesis precursor
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5
Q

How are fats carried around the body and why?

A

Lipoproteins because they have detergent like properties

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6
Q

Simple lipid examples

A

Fats, oils, wax’s

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7
Q

complex lipid examples (contain other groups)

A

Phospholipids, glycolipids, lipoproteins

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8
Q

Fats other roles in the body (non energy related)

A
  • Myelin sheath (insulator)

- bio acid production

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9
Q

Lipoproteins structure related to role

A

Hydrophilic outside hydrophobic inside (for the lipid storage)

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10
Q

What does unesterified cholesterol do in the phospholipid layer

A

Stabilises it making it stronger and prevent tails from sticking together

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11
Q

What are the 4 main lipoproteins

A
  • Chylomicrons (ULDL)
  • VLDL
  • LDL
  • HDL
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12
Q

Chylomicrons (ULDL) characteristics

A
  • Ultra low density lipoproteins
  • 90% TAG 10% CE
  • Lowest % protein highest % lipid
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13
Q

Where are Chylomicrons made

A

Small intestine

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14
Q

Very low density lipoproteins role and production site

A
  • Carry TAG, CE

- Made in liver

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15
Q

Low density lipoproteins characteristics

A
  • Only carry CE

- ‘bad’

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16
Q

High density lipoproteins characteristics

A
  • Only carry CE
  • ‘good’
  • Highest % proteins
  • Higher density
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17
Q

What does postprandial mean

A
  • Fed state
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18
Q

Journey of Dietary TAG (ingestion to blood overview)

A
  • Digested & absorbed in SI
  • TAG packaged into Chylomicrons
  • Carried in lymph to blood via subclavian vein
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19
Q

Where do chylomicrons in the blood travel to

A

Extra hepatic (non liver) tissues

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20
Q

What happens when chylomicrons reach blood vessel walls of muscle/adipose tissues

A
  • Docks into lipoprotein lipase enzyme
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21
Q

What does Lipoprotein lipase (LPL) do?

A
  • breaks down TAG (in the chylomicrons) releasing FA’s and glycerol
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22
Q

What happens to the products of LDL once they are in the tissue

A

Repackaged into TAG and stored in the tissue

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23
Q

What is chylomicron called after losing most of it TGA and what happens to it

A
  • Chylomicron / lipoprotein remnant

- it is transported to the liver and broken down

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24
Q

What happens to cholesterol from chylomicron remnant

A

Joins pool of cholesterol in the liver

- can be used to make bile for digestion where it will then be reabsorbed

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25
Q

What is de novo synthesis

A

production of cholesterol in the liver from other stuff

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26
Q

How does cholesterol get from liver to tissues for use

A

packaged into LDL some is taken up and some is transported back to the liver as HDL

27
Q

What happens to excess CHO and why (de novo synthesis)

A

it is converted into TAG in the liver and stored because we can only stored a finite amount of CHO

28
Q

How is excess fat removed from the liver

A

packaged as VLDL and sent to peripheral tissues for stored

remnants re-joins the system back in the liver

29
Q

What is catabolic state

A

breaking down state

30
Q

What happens during catabolic state (lipids)

A
  • Liver produces VLDL (TAG) to supply muscles where it is hydrolysed
  • Adipose tissues breaks down its TAG into FA for transport
  • Muscle is supplied with lots of fatty acids
31
Q

What is albumin and what does it do

A

a protein in the blood that carries fatty acids

32
Q

What happens to glycerol following TAG breakdown

A

returns to liver and undergoes gluconeogenesis forming glucose

33
Q

4 main sites/process of fatty acid regulation

A
  • Lipolysis of triacylglycerol to form free fatty acids
  • Re-esterification of FA
  • Acyl-CoA transport into mitochondria
  • Availability of FAD & NAD for Beta oxidation
34
Q

What are adipocytes and how are they specilised

A
  • cells in adipose tissue

- basically all fat just for storage

35
Q

Fat storage number facts

A
  • 60 kg w/ 10% body fat

= 6kg fat = 6000g = 54000 kcal = 25 days of energy

36
Q

lipolysis definiton

A

the breakdown of fats and other lipids to releases fatty acids

37
Q

how is lipolysis regulated?

A

by hormone sensitive lipase (HSL)

38
Q

HSL regulation (inactive/active)

A
  • Protein kinase adds phosphate group making it active

- Phosphatase removes phosphate group

39
Q

What substances increase HSL activation and why would want this

A
  • calcium ions, adrenaline, amp (exercise)

- growth hormone, cortisol (stress)

40
Q

what substances increases inactive HSL and why would you want this

A
  • Insulin (after eating for storage)
41
Q

re-esterification overview (happens in adipocytes)

A
  • lipolysis stimulated
  • FA & glycerol produced (glycerol leaves cell)
  • FA form Fatty acyl-CoA
  • Joins with glycerol P (from glycolysis) reforming TAG
42
Q

what is re-esterification

A

remaking of TAG following breakdown (not helpful)

43
Q

What does exercise causes in relation to lipolysis and what effect does this have?

A
  • increases lipolysis
  • reduces glucose uptake (no insulin)
  • means there is less glycerol P for re-esterification leading to a FA build up and then it leaving the cell and entering the blood stream
44
Q

How do fatty acids get across cell membranes (carrier protein names)

A
  • Fatty acid binding protein (FABP)
  • Fatty acid translocase (FAT/CD36)
  • Fatty acid transport protein (FATP)
45
Q

How does FA get into muscle interstitial fluid from blood

A
  • into interstitial fluid by lipoprotein lipase on membrane (from LDL/HDL)
    or deposited by albumin
46
Q

How does FA get into muscle sarcoplasm from interstitial fluid

A

moves down conc grad going through FAT CD36 (site of regulation)

47
Q

What happens to FA once inside muscle sarcoplasm

A

is synthesised into fatty-acyl-CoAs

48
Q

How is FA storage in muscle

A

the fatty-acyl-CoAs become incorporated into other lipids pool eg intermuscular triglyceride droplet (IMTG)

49
Q

Role of IMTH and where is it located

A
  • readily available fuel source for mitochondria (broken down same way as in adipose tissue)
  • found close to mitochondria in sarcoplasm
50
Q

features of mitochondria membrane

A

Outer - lipid permeable

Inner - lipid impermeable

51
Q

How do FA get into the mitochondria (carnitine shuttle overview)

A
  • CPT 1 (on outer membrane) attaches carnitine to acyl, (CoA is removed) = acylcarnitine
  • then travels through inner membrane by CACT into mitochondrial matrix
  • CPT2 removes carnitine and attaches CoA
52
Q

What happens to Acyl-CoA once inside the mitochondrial matrix

A

undergoes beta oxidation (making acetyl CoA for the TCA cycle & co enzymes for the ETC)

53
Q

What happens to fat oxidation during prolonged exercise (maintained intensity)

A
  • it increase over time as CHO oxidation decreases (depleted stores)
54
Q

What happens to FA conc during prolonged exercise

A
  • initial small dip - as FA is taken up by muscle & slow FA mobilisation from adipose
55
Q

When does FA conc increase during prolonged exercise

A

when insulin is reduced and adrenaline is increased so more HSL is activated

56
Q

Why does fatty acid oxidation increase

A

increase FA conc in blood results in greater flux so more FA for muscle to taken up meaning more FA oxidation

57
Q

How does ^ FA oxidation effect CHO oxidation (overview)

A
  • ^ FA flux = ^ acetyl-coA
= PDH inhibited
= ^ citrate accumulation
 = PFK inhibited
= G6P accumulation
= gluconeogenesis is inhibited
- less conc grad so less glucose is taken up
58
Q

How does high fat diet for long period or before exercise effect performance (^ FA flux)

A
  • good for ultra endurance (^ muscle/liver glycogen stores as fat will because earlier)
  • bad for high intensity
59
Q

Why are LDL’s so bad

A
  • has a longer half life than VLDL/chylomicrons (2 days compared to 2 hours
  • increased time means more likely to be damaged (smoking, sugar ect)
60
Q

What does damage to LDL lead to

A

increased affinity to bind to receptor on macrophages

macrophages don’t have a CE sensor so they keep taking it up until they become a foam cell

61
Q

what does an accumulation of foam cells cause

A

build up on blood vessels walls leads to fatty streaks/deposits (atherosclerosis)

can lead to plaque

= blood vessels obstructed (CVD)

62
Q

Why is HDL good

A

^ HDL = decrease CVD risk

HDL will dock to foam cells and remove excess CE and take it to liver for proper use

63
Q

lifestyle modifications related to lipid health

A

exercise = ^ HDL

diet, drug eg plant sterols

Y1 Nutrition & metabolism (11 decks)

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