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Biochemistry Year 1 > Lipids and lipid metabolism > Flashcards

Lipids and lipid metabolism Flashcards

1
Q

What are the eight types of dietary fats?

A

SCFAs; SCFAs (C12-C18); MUFAs; PUFAs (n-6); PUFAs (n-3); cholesterol; phospholipids; trans fats

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2
Q

What are sources of SCFAs?

A

Milk, milk products, butter

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3
Q

What are sources of SCFAs (C12-C18)?

A

Meat, animal foods and fats, coconut and palm oils

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4
Q

What are sources of MUFAs?

A

Olive and rapeseed oils

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5
Q

What are sources of PUFAs (n-6)?

A

Sunflower and soybean oils, meat, eggs, nuts

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6
Q

What are sources of PUFAs (n-3)?

A

Oily fish

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7
Q

What are sources of cholesterol?

A

Eggs, organ meats

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8
Q

What are sources of phospholipids?

A

Animal foods, eggs

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9
Q

What are sources of trans-fats?

A

Ruminant animals, hydrogenated fats in manufactured goods

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10
Q

Where are fats stored?

A

Muscle fibres; within circulation; adipose tissues (subcutaneous and internal fats); adipocytes / lipocytes

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11
Q

How much ATP is released per TG?

A

~400ATP

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12
Q

How does fat energy storage compare to carbohydrate energy storage?

A

Fat accounts for ~80% (50,000-100,000kcal) of energy stored in body; carb energy reserve is just 2% of fat energy reserve (2000kcal)

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13
Q

Where is most glycogen stored?

A

In muscles

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14
Q

What is the order of quantity of energy storage?

A

Fats > proteins > carbs

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15
Q

What are the three classes of lipids?

A

Neutral, compound, and derived lipids

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16
Q

What are neutral lipids?

A

FAs and TGs; comprise of glycerol backbone + 3FAs

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17
Q

What are compound lipids?

A

Plipids; are ampithatic (hydrophobic and philic)

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18
Q

What are derived lipids?

A

Steroids and sterols; cholesterol (6C ring + 5C ring)

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19
Q

What is the implication of a longer chain FA?

A

More solid @RTP

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20
Q

What do saturated FAs stimulate?

A

Stimulates liver to form cholesterol

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21
Q

What are trans fats?

A

Form due to processing (heat, light, hydrogenation); have rigid double bonds; trans fats are trans (H and C on opposite sides @ C=C double bond); trans nature means chain is straight and less likely to be liquid; have structure of unsaturated, with properties of saturated; proposed to be better for health

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22
Q

What are examples of

essential FAs?

A

3-linolenic (n-3) and linoleic (n-6) acid

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23
Q

What do 3-linolenic and linoleic acids do?

A

Play a role in regulation of gene expression; involved in signal transduction; metabolites produce compounds involved in cell function, inflammation, and immune function

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24
Q

What are plipids?

A

Glycerol + 2FAs + Pi; are amphipathic; have hydrophobic tail and hydrophilic head; can be unsaturated or saturated; form plipid bilayer and lipoproteins

25
Q

What do lipoproteins do (general)?

A

Carry TGs around in blood within them

26
Q

What are four types of lipoproteins?

A

Chylomicrons, VLDL, LDL, HDL

27
Q

What do chylomicrons do?

A

Have TGs packaged into them; allow absorption of TGs in small intestines; main transport of FAs to body tissues

28
Q

What do VLDLs do?

A

Collect lipid droplets; transport FAs to body tissues

29
Q

What do LDLs do?

A

Transports large amounts of cholesterol

30
Q

What do HDLs do?

A

Collect excess cholesterol and take back to liver; have more protein and less lipid than LDLs

31
Q

What are three ways that lipids can be mobilised?

A

Diet –> TGs –> chylomicrons –> lipolysis by lipoprotein lipase –> energy freed from lipids.
Adipose cells/ tissue –> released by hormone sensitive lipase –> form glucagon –> more FFAs and albumin.
Synthesised from liver –> convert excess glucose –> FFAs –> TGs and cholesterol

32
Q

How are lipids metabolised within the post-prandial period?

A

In mouth, saliva contains lipase; FAs cleaves off TGs; slow process due to watery environment. In stomach, acid-stable lipase further hydrolyses TGs. In small intestine, TGs form past-like substance (lipid droplets) due to hydrophobic nature; gall bladder releases bile salts; bile salts emulsify droplets; pancreatic lipase into duodenum; pancreatic lipase further hydrolyses TGs; LCFA + MGs liberated; MGs and FFAs form micelles; micelles release FFAs and MGs into lining of epithelial cells; FAs and MGs diffuse into villi epithelial cells; FAs + MGs –> TGs due to watery environment; TGs packaged into chylomicrons; chylomicrons diffuse into lymph; lymph deposits chylomicrons in circulatory system within subclavian veins

33
Q

What happens to lipids once in the blood?

A

Chylomicrons travel to tissues; lipoprotein lipase of extrahepatic tissues release FAs within chlyomicrons; FAs are: taken up by adipose for storage/ taken into muscle for fuel or storage as intramuscular TG/ excess FAs cleaved and trasported back to liver, carried by albumin and recycled in a VLDL –> TG

34
Q

What occurs to lipids in the post-absorptive state/ when fasting?

A

Are no chlyomicrons; liver produces VLDLs; VLDLs carry TG; drop in glucose = drop in insulin, increase in glucagon; glucagon stimulates (via hormone sensitive lipase) adipose cells to release FAs into blood; albumin is released by liver; FAs bind to albumin; liver takes up FAs which are picked up by LDL and HDL; liver breaks down fats for gluconeogenesis

35
Q

How is FA utilisation regulated?

A

Transport of acyl-CoA esters into mitochondria; availability of FAD and NAD for beta-oxidation; lipolysis of TG –> FFAs (analogous to mobilisation of glycogen); resterification of FAs; mobilisation from adipose tissue

36
Q

What is beta oxidation?

A

The separation of C chain at the 2nd (beta) carbon

37
Q

How are FAs transported to target cells?

A

Adipose stores TGs; lipase breaks down TGs –> MG + FAs; FAs enter blood; FA enters cell via transporter; FA enters mitochondrion

38
Q

What cells cannot metabolise FAs?

A

Brain cell or RBCs

39
Q

How do FAs enter the mitochondrial matrix of the target cell?

A

Acyl-CoA synthase catalyses FFA –> acyl-CoA; acyl-CoA through porins of outer membrane; acyl-CoA into intermembrane space; carnitine palmitoyl transferase 1 on outer membrane attaches carnitine + acyl-CoA –> acyl carnitine (carnitine shuttle); CoA back into cytoplasm; acyl carnitine through carnitine acylcarnitine translocase on inner membrane into matrix; carnitine palmitoyl transferase 2 attaches CoA + acyl –> acyl-CoA; carnitine regenerated and back to intermembrane space

40
Q

What regulates rate of FAO at CAPT1?

A

Glycolytic flux

41
Q

How does beta oxidation occur?

A

Fatty acyl CoA has two C atoms removed from FA –> acetyl CoA + remaining FA: involves dehydrogenation (simultaneously reducing FAD); hydration; dehydrogenation (simultaneously reducing NAD); thiolysis (cleavage reaction catalysed by thiolase). Remaining FA re-enters pathway

42
Q

Why is the actual energy yield from FAs not as much as the theorised?

A

Due to activation of FAs and processes in Krebs and ETC

43
Q

Roughly how many ATP are produced from each acetyl-CoA, NADH, and FADH2?

A

Acetyl-CoA ~10ATP (perfect would be 12).
NADH ~2.5 (perfect would be 3).
FADH2 ~1.5 (perfect would be 2)

44
Q

How many ATP are used in FA activation?

A

2

45
Q

How nutrients interconverted?

A

Gluconeogenesis at the liver: glycerol, lactate and certain amino acids –> glucose; Lipogenesis at the liver and adipose cells: glucose and amino acids –> lipids

46
Q

How is lactate converted to glucose?

A

Cori cycle: 2 lactate –> 2 pyruvate + glucose

47
Q

How does carb oxidation change during prolonged exercise?

A

Significantly reduces over a three hour time span

48
Q

How does fat oxidation change during prolonged exercise?

A

Significantly increases from onset of exercise

49
Q

What substrate is responsible to largest energy expenditure?

A

Muscle glycogen - is used until it runs out

50
Q

What is maximal fat oxidation?

A

Fat max: consume most fat @65% VO2max

51
Q

Where does the range of fat max lie in regards to HR?

A

~60-80% HRmax

52
Q

How does training status affect fat max?

A

%VO2max where fat max lies remains the same; fat max rate is increased in higher trained individuals

53
Q

How does training affect substrate utilisation?

A

Endurance training increases use of intramuscular fat stores; less carbs are used

54
Q

How does gender affect fat max?

A

Females’ fat max occurs at higher %HRmax; females’ fat max rate is higher

55
Q

How does carb intake affect fat oxidation?

A

Consumption of carbs pre-exercise significantly reduces fat oxidation, particularly on intramuscular TGs

56
Q

How does cycling affect fat max compared to running on a treadmill?

A

Oxidise much lower fats; fat max similar both when on treadmill and bike

57
Q

How does exercise affect glycogenolysis?

A

Increased exercise intensity increases glycogenolysis in almost a linear relationship

58
Q

Why is fat oxidation not sufficient at high intensity?

A

70-90% VO2max needs ~1mol ATP/min, but maximal rate of rate oxidation is only ~0.4 mol ATP/min

59
Q

How does carb oxidation reduce fat oxidation at increased exercise intensity?

A

Increased plasma FAs does not increase fat oxidation during high intensity + main effect is on IMTG = limitation within muscle cell. Only oxidation of LCFAs is impaired = carnitine shuttle and beta oxidation are limiting = CoA, NAD, carnitine all needed for processes. CoA, NAD, carnitine reduced during high intensity exercise with increase in carb oxidation = source of reduced fat oxidation

Biochemistry Year 1 (23 decks)

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