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Nutrition & metabolism > fat metabolism > Flashcards

fat metabolism Flashcards

1
Q

what are fatty acids and what are the 3 types of them?

A

organic chains of C,H and O

number and bonding of carbon atoms:

  1. saturated - 0 double bonds
  2. monounsaturated - 1 double bond
  3. polyunsaturated - >1 double bond
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2
Q

what is the 5 stage digestion of fat?

A
  1. lipids emulsified by the bile
  2. lipases break down triglycerides into fatty acids and monoglycerides
  3. packaged into micelles that are absorbed by microvilli
  4. converted back into triglycerides which aggregate with cholesterol, protein and phospholipids to form chylomicrons
  5. move into lymph capillary which transports them to rest of body
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3
Q

what is the postprandial state of fat?

chylomicrons
what happens to fatty acids

A

postprandial = after a meal

lymphatics secrete chylomicrons into subclavian vein

dock onto lipoprotein lipase of extrahepatic tissues, which release fatty acids and glycerol

fatty acids taken up by adipose tissue for storage, into muscle to be used as fuel or stored as intramuscluar triacylglycerol for later use or taken up by liver and recycled as VLDL and sent to adipose for storage

if stored: esterified with glycerol-3-phosphate

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4
Q

what is an extrahepatic tissue?

A

non-liver tissue

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5
Q

what type of lipoproteins are chylomicrons, VLDL, LDL and HDL?

A

chylomicron - ultra low density lipoprotein

VLDL - very low density lipoprotein

LDL - low density lipoprotein

HDL - high density lipoprotein

density = ratio of protein to lipid
low = lots more lipid than protein
high = higher ratio of protein to lipid
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6
Q

what occurs in the postabsorptive state?

A

all fat digested and absorbed

no chylomicrons so liver produces VLDL to carry triacylglycerol (TAG)

stored in adipose tissue and hydrolysed into fatty acids and glycerol by hormone sensitive lipase (HSL) and released

fatty acids either turned back into triacylglycrol for storage (reseterification)
or bind to albumin to prevent coalescing (fatty acids binding together) and allow transport into aqueous blood

used by other tissues as energy substrate

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7
Q

what happes to TAG during exercise or stress?

A

mobilised for oxidation into fatty acids

similar to mobilisation of glycogen as occurs under similar circumstances and hormonal control

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8
Q

what is lipase a general term for?

A

any enzyme which hydrolyses TAG into fatty acids and glycerol

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9
Q

when is HSL activated and deactivated?

A

hormone sensitive lipase which stimulates lipolysis

activated: when phosphorylated by protein kinases (activated by exercise as insulin levels fall)
deactivated: in presence of phosphatase (activated by insulin in anabolic state)

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10
Q

describe fatty acid transport across cell membranes?

A

dependent upon plasma fatty acid conc as more in circulation then more fat transported into cell as moves down concentration gradient

flip-flop and carrier mediated process:

  1. fatty acid binding protein (FABP)
  2. fatty acid translocase - most important (FAT/CD36)
  3. fatty acid transport protein (FATP)
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11
Q

what happens to fatty acids once inside the cell?

A

become activated by acyl-CoA synthetase ezymes
to fatty-acyl-CoAs

can then be moved aorund cell

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12
Q

what is the postpradial state of cholesterol?

A

cholesterol packaged into LDL and carried to tissues

taken away by HDL and excess entered into bile

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13
Q

where is fat stored in the body?

A

lots more stored in adipose tissue (months of energy) than muscles and liver

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14
Q

what is lipolysis?

A

break down of lipids within adipose tissue to release free fatty acids to transport to other tissues for energy

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15
Q

what are adipose tissue cells called and what do they contain?

A

adipocytes

only thing within is fat (TAG)

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16
Q

what are the 2 uses of fatty acids inside the cell?

A

either stored as TAG in lipid droplets

or utilised in mitochondria for energy

lipid droplet bound to mitochondria so readily available food source

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17
Q

what stimulates protein kinase in muscles?

why is it important?

A

calcium
adrenaline
AMP

so fatty acids from TAG can be used for energy

18
Q

what are the 2 membranes of mitochondria and what does this mean for fatty acid transportation?

A

1) inner impermeable to fatty acids -
CPT1 - acyl group binds to carnitine then can cross membrane
CPT2 converts back to acyl-CoA

2) permeable to fatty acids

19
Q

briefly describe beta-oxidation?

A

purpose to turn long chain acyl-CoA into many acetyl-CoA molecules that can enter TCA cycle then electron transport chain

several of the enzymes involved have co-factors which are required for enzymatic reactions (in limited supply so limits rate of beta oxidation)

20
Q

what does carbohydrate oxidation do during prolonged exercise of same intensity?

A

declines over time - requires same ATP demand throughout when same intensity

as shown through decline in contribution of blood glucose and muscle glycogen

21
Q

what does fat oxidation do during prolonged exercise of same intensity?

A

increases over time in order to meet energy (ATP) demand

as shown by increase in circulating plasma fatty acid availability so muscles flooded with fat

22
Q

how to work out kJ energy from fat and carb oxidation?

A

fat - g x 39.4

carb - g x 15.6

23
Q

why is there an intial drop in plasma fatty acids at start of exercise?

A

slow mobilisation of fatty acids lipolysis (after reach certain conc) from adipose tissue
uptake of fatty acids from working muscles

24
Q

describe what happens when fatty acid flux increases in relation to carbohydrate oxidation?

A

increased fatty acid flux will increase acetyl-CoA which

inhibits PDC (pyruvate dehydrogenase - transport of pyruvate into mitochondria to be oxidised) so carbohydrate oxidation

acetyl CoA will form citrate which inhibits PFK which inhibits glycolysis so carbohydrate oxidation

25
Q

describe relationship between exercise intensity and fat oxidation rate?

A

as exercise intensity increases, energy demand increases so fat oxidation increases

as intensity increases even higher, oxidation plateaus and even declines to become very low (after 65% VO2 max)

26
Q

what is the peak of fat oxidation rate when exercising?

A

at 60-65% VO2 max

27
Q

what happens in relative contributions of fat during increased fat oxidation?

A

as fat oxidation goes up

intramuscular fat contribution increases and contribution of plasma fatty acid from adipose tissue decreases

28
Q

what happens to ATP resynthesis during an increasing number of metabolic reactions?

A

more metabolic reactions reduces maximal rate of ATP resynthesis (how fast they can generate ATP)

quickest resynthesis = ATP and PCr (immediate energy sources as only require 1/2 reactions)

followed by muscle glycogen, liver glycogen and fatty acids (require more transport and metabolic reactions to produce ATP)

29
Q

why can’t exercise at 70-90% VO2 max be facilitated by fat oxidation alone?

A

demands around 1 mol ATP/min but fatty acids maximal rate of ATP resynthesis is only 0.4 mol ATP/min

so need carbohydrate as well

30
Q

what are the contributions to energy during 85% exercise intensity?

A

contribution of muscle glycogen the most, followed by plasma glucose then plasma fatty acids and triacylglycerols

31
Q

why increasing exercise intensity reduce fat oxidation?

A

limitation of how fat used within muscle cell: main effect on IMTG and increasing plasma FA doesn’t increase fat oxidation at high exercise intensities

only oxidation of long chain fatty acids impaired which are rate limited by carnitine shuttle and beta oxidation (requires CoA, NAD and carnitine which decline during high energy exercise due to increase in oxidation of carbohydrates)

32
Q

describe the carnitine shuttle?

A

carnitine translocating fats into mitochondria

amount of carnitine in muscle fixed

33
Q

describe the acetyl-CoA buffer?

A

high intensity exercise means flux through PDC reaction is greater than TCA cycle

increases acetyl-CoA and depletes CoA

caritine esterifies with excess acetyl groups to form acetylcarnitine

partially maintais CoA but depletes carnitine

34
Q

describe the acetyl-CoA buffer and it’s role in increasing CoA?

A

high intensity exercise means flux of acetyl-CoA through PDC reaction is greater than requirements of TCA cycle (carbohydrate oxidation)

depletes CoA in mitochondria as needed to form acetyl-CoA

carnitine esterifies with excess acetyl groups to form acetylcarnitine to free up CoA

depletes carnitine so can’t be used for fat oxidation

35
Q

what will a reduction in carnitine or CoA reduce?

A

the flux through the carnitine shuttle and fatty acid oxidation and beta oxidation

36
Q

what will reduction in FAD NAD or CoA reduce?

A

flux through beta oxidation therefore fatty acid oxidation

as used in PDC pathway instead to aid carbohydrate oxidation

37
Q

what are FAD NAD and CoA required for and where does this reaction occur and what does it reduce?

A

required for the PDC reaction

increasing PDC flux will reduce their availability for beta oxidation so reduction in fat oxidation

occurs within mitochondria

38
Q

what occurs regarding oxidation at 60-70% VO2 max?

A

decrease in fat oxidation

reciprocal increase in glycotic flux (inhibits fat oxidation at level of carnitine shuttle or beta oxidation) and carbohydrate oxidation

39
Q

what happens in relation to carb oxidation if you have a high fat diet or eat fat just before exercise?

A

greater rate of fatty acid flux and reduced rate of carb oxidation

spare muscle and liver glycogen stores

BUT not good for high intensity exercise

40
Q

why does glycogenolysis increase during increased exercise intensity?

A

as exercise intensity increases and ATP demands increases, more AMP produced so stimulates increase in glycogenolysis

leading to increase in carbohydrate oxidation

Nutrition & metabolism (20 decks)

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