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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
What is de novo synthesis
production of cholesterol in the liver from other stuff
26
How does cholesterol get from liver to tissues for use
packaged into LDL some is taken up and some is transported back to the liver as HDL
27
What happens to excess CHO and why (de novo synthesis)
it is converted into TAG in the liver and stored because we can only stored a finite amount of CHO
28
How is excess fat removed from the liver
packaged as VLDL and sent to peripheral tissues for stored | remnants re-joins the system back in the liver
29
What is catabolic state
breaking down state
30
What happens during catabolic state (lipids)
- 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
What is albumin and what does it do
a protein in the blood that carries fatty acids
32
What happens to glycerol following TAG breakdown
returns to liver and undergoes gluconeogenesis forming glucose
33
4 main sites/process of fatty acid regulation
- 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
What are adipocytes and how are they specilised
- cells in adipose tissue | - basically all fat just for storage
35
Fat storage number facts
- 60 kg w/ 10% body fat | = 6kg fat = 6000g = 54000 kcal = 25 days of energy
36
lipolysis definiton
the breakdown of fats and other lipids to releases fatty acids
37
how is lipolysis regulated?
by hormone sensitive lipase (HSL)
38
HSL regulation (inactive/active)
- Protein kinase adds phosphate group making it active | - Phosphatase removes phosphate group
39
What substances increase HSL activation and why would want this
- calcium ions, adrenaline, amp (exercise) | - growth hormone, cortisol (stress)
40
what substances increases inactive HSL and why would you want this
- Insulin (after eating for storage)
41
re-esterification overview (happens in adipocytes)
- lipolysis stimulated - FA & glycerol produced (glycerol leaves cell) - FA form Fatty acyl-CoA - Joins with glycerol P (from glycolysis) reforming TAG
42
what is re-esterification
remaking of TAG following breakdown (not helpful)
43
What does exercise causes in relation to lipolysis and what effect does this have?
- 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
How do fatty acids get across cell membranes (carrier protein names)
- Fatty acid binding protein (FABP) - Fatty acid translocase (FAT/CD36) - Fatty acid transport protein (FATP)
45
How does FA get into muscle interstitial fluid from blood
- into interstitial fluid by lipoprotein lipase on membrane (from LDL/HDL) or deposited by albumin
46
How does FA get into muscle sarcoplasm from interstitial fluid
moves down conc grad going through FAT CD36 (site of regulation)
47
What happens to FA once inside muscle sarcoplasm
is synthesised into fatty-acyl-CoAs
48
How is FA storage in muscle
the fatty-acyl-CoAs become incorporated into other lipids pool eg intermuscular triglyceride droplet (IMTG)
49
Role of IMTH and where is it located
- readily available fuel source for mitochondria (broken down same way as in adipose tissue) - found close to mitochondria in sarcoplasm
50
features of mitochondria membrane
Outer - lipid permeable | Inner - lipid impermeable
51
How do FA get into the mitochondria (carnitine shuttle overview)
- 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
What happens to Acyl-CoA once inside the mitochondrial matrix
undergoes beta oxidation (making acetyl CoA for the TCA cycle & co enzymes for the ETC)
53
What happens to fat oxidation during prolonged exercise (maintained intensity)
- it increase over time as CHO oxidation decreases (depleted stores)
54
What happens to FA conc during prolonged exercise
- initial small dip - as FA is taken up by muscle & slow FA mobilisation from adipose
55
When does FA conc increase during prolonged exercise
when insulin is reduced and adrenaline is increased so more HSL is activated
56
Why does fatty acid oxidation increase
increase FA conc in blood results in greater flux so more FA for muscle to taken up meaning more FA oxidation
57
How does ^ FA oxidation effect CHO oxidation (overview)
- ^ 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
How does high fat diet for long period or before exercise effect performance (^ FA flux)
- good for ultra endurance (^ muscle/liver glycogen stores as fat will because earlier) - bad for high intensity
59
Why are LDL's so bad
- 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
What does damage to LDL lead to
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
what does an accumulation of foam cells cause
build up on blood vessels walls leads to fatty streaks/deposits (atherosclerosis) can lead to plaque = blood vessels obstructed (CVD)
62
Why is HDL good
^ HDL = decrease CVD risk HDL will dock to foam cells and remove excess CE and take it to liver for proper use
63
lifestyle modifications related to lipid health
exercise = ^ HDL diet, drug eg plant sterols

Y1 Nutrition & metabolism (11 decks)

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