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ESS1606 Nutrition and metabolism > Fat metabolism > Flashcards

Fat metabolism Flashcards

1
Q

FAs

A
  • Organic chains of C, H, and O
  • Categorised based on the number and bonding of carbon atoms
  • Saturated (0 double bonds)
  • Monounsaturated (1 double bond)
  • Polyunsaturated (>1 double bond)
  • n = omega = number of carbons from methyl end
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2
Q

Posprandial state

A

• Postprandial = after a meal
• The lymphatics secrete chylomicrons into subclavian vein
• Chylomicrons dock onto lipoprotein lipase (LPL) of extrahepatic (non-liver) tissues, which releases fatty acids (FA) and glycerol
• These FA are taken up by adipose tissue for storage, or into the muscle either for utilisation as a fuel, or stored as intramuscular triacylglycerol (TAG) for later use
• If stored, FA are esterified with glycerol-3-phosphate
• Some FA are also taken up by the liver and recycled in a VLDL
DIAGRAM

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3
Q

Postabsorptive state

A

• In the fasted (postabsorptive) state, there are no chylomicrons so the liver produces very low density lipoproteins (VLDL) to carry TAG
• TAG stored within adipose tissue is hydrolysed (broken down) into FA and glycerol by hormone sensitive lipase (HSL)
• These FA are transported out of the adipocyte, although some are re- esterified (turned back into TAG for storage)
• The released FA bind to albumin to prevent coalescing and allow transport in aqueous blood
• The fatty acids are then utilised by other tissues as an energy substrate
DIAGRAM

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4
Q

Reg of FA utilisation

A

• Lipolysis of triacylglycerol to form free fatty acids
• Re-esterification of the fatty acids, or alternatively, their mobilisation
from adipose tissue
• Transport of the acyl-CoA esters into the mitochondrion
• Availability of FAD and NAD for B-oxidation

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5
Q

FA lipolysis and mobilisation from adipose tissue

A
  • Similar to post-absorptive state, during exercise or stress TAG are mobilised for oxidation
  • Analogous to mobilisation of glycogen as occurs under similar circumstances and under hormonal control
  • 60 kg individual with 10% body fat • 6 kg fat = 54,000 kcal
  • 25 days food energy
  • Total glycogen around 3000 kcal
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6
Q

Lipolysis

A

Hormone Sensitive Lipase (HSL)
• Lipase = general term for any enzyme which hydrolyses TAG into FA and glycerol
• HSL is activated when phosphorylated by protein kinase(s)
DIAGRAM

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7
Q

Lipolysis v re-esterification

A

DIAGRAM

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8
Q

FA transport across cell membranes

A
  • ‘Flip-flop’ and carrier mediated process
  • Uses functional carriers
  • Once inside the cell fatty acids then become activated by a family of acyl- CoA synthetase enzymes to fatty-acyl-CoAs
  • Once activated acyl-CoA (e.g. palmitoyl-CoA) can either undergo incorporation into other lipid pools or oxidation by mitochondria
  • Once such lipid pool in intramuscular triacylglycerol (IMTG) droplets
  • Synthesis similar to adipose tissue triacylglycerol droplets
  • IMTG is a readily available fuel source for mitochondria
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9
Q

Lipolysis of IMTG

A

DIAGRAM

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10
Q

Carnitine shuttle

A

DIAGRAM

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11
Q

B-oxidation

A

DIAGRAM
• Its purpose is to turn acyl-CoA into many acetyl-CoA molecules
• Each cycle removes a 2-carbon fragment from acyl-CoA to release
1 acetyl-CoA molecule
• The acetyl-CoA then enters the TCA cycle
• The H+ enter the ETC
• Acyl-CoA then returns to the top of the cycle and the process is repeated until all the carbons in the fatty acid chain are consumed

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12
Q

Fat ox during prolonged ex

A

• Increase to meet energy demand
• kJ energy from fat ox = g x 39.4
• kJ energy from carb ox = g x 15.6
o Same energy contribution

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13
Q

Plasma FA concentration during prolonged ex

A
  • Regulates lipolysis
  • Exponentially increases
  • Plasma adrenaline also increase and insulin falls
  • Initial drop in plasma DA reflects slow mobilisation of FA from adipose tissue and uptake of FA from working muscles
  • Increased FA flux (rate molecule passes through several reactions) will increase acetyl CoA
  • Increases acetyl CoA will inhibit PDC (pyruvate dehydrogenase complex) and carb ox
  • Increasing acetyl CoA will increase citrate, which inhibits PFK
  • Inhibiting PFK will inhibit glycolysis and carb ox
  • Accumulation G6P – inhibit glycogenolysis – inhibit glucose passing down grad
  • Better to rely on fat – unlimited store – try and spare glycogen
  • Not good for high intensity ex
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14
Q

Fat ox and ex intensity

A

(Reg how much fat used during ex)

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15
Q

Metabolic demands of ex

A
  • As ex intensity increases, ATP demand of contraction increases
  • Ex between 70-90% VO2 max requires ATP demand of around 1 mol ATP/min
  • Clearly cannot be met by fat ox alone (max rate of 0.4 mol ATP/min)
  • Why does fat ox decline?
  • Avail of substrates during ex
  • Max rate of utilisation
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16
Q

Increase in carb ox coincides with decline in fat ox

A

Change in carb depends on rate glycogen utilisation

17
Q

Why does increase in carb ox with increasing ex intensity reduce fat ox?

A
  • Increase glycogenolysis
  • Main effect is on IMTG, which would suggest limitation with muscle cell
  • If increase plasma FAs doesn’t increase fat ox during high intensity ex, suggesting limitation in muscle cell
  • Only ox of long chain FAs impaired which are limited by carnitine shuttle and B-ox
  • CoA, NAD and carnitine required for these processes and they decline during high intensity ex with increase in carb ox
18
Q

Carnitine shuttle

A

Fixed amount in muscle

19
Q

Glycolytic flux increase with increasing ex intensity

A

Increased flux through glycolysis increases rate of lactate accumulation and pyruvate ox (PDC flux)

20
Q

Acetyl CoA buffer

A
  • At high intensity ex flux through PDC reaction greater than TCA cycle flux
  • Increases acetyl CoA and depletes CoA
  • Carnitine esterifies with excess acetyl groups to form acetylcarnitine
  • Partially maintains CoA, but depletes carnitine
  • Imp to allow continuation carb ox
21
Q

Pyruvate dehydrogenase complex (PDC)

A
  • NAD, FAD and CoA required for PDC reaction, and increasing PDC flux will reduce avail to B-ox
  • All reactions occur within mitochondria, which have limited stores of NAD, FAD and CoA
  • Easier to ox carb than fat
  • Want to use just carb during high intensity ex
22
Q

Integration of fat and carb met

A
  • With increase in ex duration at same intensity, plasma FAs increase from adipose tissue (slow process) and FA transport into muscle increases
  • Increase fat ox and inhibits carb ox, likely at level of PDC and PRK
  • With increase in ex intensity above 60-70% VO2 max, decrease in fat ix
  • Coincides with reciprocal increase in glycolytic flux and carb ox
  • Increase in glycolytic flux inhibits fat ox at level of carnitine shuttle/B-ox, due to reducing avail of mitochondrial carnitine/co-factors
23
Q

Fat mobilisation and use during ex

A
  • Depending on nutritional and fitness status of indvs and ex intensity and duration, intracellular and extracellular fat supplies between 30-80% of ex energy requirement
  • 3 lipid sources supply major energy for light-to-moderate ex:
  • Fat use for energy in light and moderate ex varies with blood flow through adipose tissue (3 fold increase no uncommon) and through active muscle
  • Adipose tissue releases for FFAs to active muscle as blood flow increases with ex
  • Greater quantities of fat from adipose tissue depots participate in energy met
  • Energy contribution from intramuscular TAG ranges between 15-35% with endurance-trained men and women using largest quantity and substantial impairment in use among obese and type 2 diabetics
  • Initiation of ex produces transient initial drop in plasma FFA conc from increased uptake by active muscles and time lag in release and delivery from adipocytes
  • Increased FFA release from adipose tissue occurs through hormonal-enzymatic stimulation by SNS activation and decreased insulin levels
  • Ab adipocytes represent lively area for lipolysis compared with fat cells in gluteal-femoral region
  • When ex transitions to high intensity, FFA release from adipose tissue fails to increase much above resting levels, which eventually produces decrease in plasma FFAs
  • Increases muscle glycogen usage, with a concurrent large increase in IMTG ox
  • Considerable FA ox occurs during low-intensity ex
  • E.g. Fat combustion totally powers light ex at 25% aerobic capacity
  • Carb and fat combustion contribute energy equally during moderate ex
  • Fat ox gradually increases as ex extends to hr+ and glycogen depletes
  • Toward end of prolonged ex, circulating FFAs supply nearly 80% of total energy required
  • Hormones epinephrine, norepinephrine, glucagon and growth hormone activate hormone-sensitive lipase
  • Causes lipolysis and mobilisation of FFAs from adipose tissue
  • Ex increases plasma levels of lipogenic hormones, so active muscles receive continual supply of energy-rich FA substrate
  • Increased activity of skeletal muscle and adipose tissue lipases, inc biochem and vascular adaptations within muscle, help explain training-induced enhanced use of fats for energy during moderate-intensity ex
  • Augmented fat met in prolonged ex results from small drop in blood sugar, accompanied by decrease in insulin and increased glucagon output by pancreas as ex progresses
  • Changed reduce glucose met to further stimulate FFA liberation for energy
  • With carb depletion, ex intensity decreases to level governed by body’s ability to mobilise and oxidise fat
  • Prior ex also partitions trafficking of dietary fat fed in recovery toward direction that favours ox rather than storage
  • May explain protection against weight gain offered by regular PA
  • Co summing high fat diet for protracted period produces enzymatic adaptations that enhance capacity for fat ox during ex
24
Q

3 lipid sources supplying major energy for light-moderate ex

A

o FAs released from TAG storage sites in adipocytes and delivered slowly to muscles a FFAs bound to plasma albumin
o Circulating plasma TAG bound to lipoproteins as VLDL and chylomicrons
o TAG within active muscle itself

25
Q

Ex intensity makes a diff

A
  • Contribution of fat to metabolic mixture in ex differs depending on ex intensity
  • Moderately trained subjects, ex intensity that maximises fat burning ranges between 55 and 72% VO2 max
  • Light to mild – fat main source – plasma FFAs from adipose tissue depots
  • Increase intensity provides crossover in balance fuel use
  • Total energy from fat breakdown remains unchanged, while blood glucose and muscle glyc supplied added energy for more intense ex
  • No diff in total energy from fats during ex at 85% of ma and ex at 25% of max
  • Carb major fuel source during intense aerobic ex
26
Q

Nutritional status plays a role

A
  • Dynamics of fat breakdown/synthesis depend on avail of ‘building block’ FA molecules
  • After meal, when energy met low, digestive processes increase FFA and TAG delivery to cells
  • Increased fat delivery promotes TAG synthesis through esterification
  • With moderate ex, increased use FAs for energy reduces as conc in active cells, thus stimulating TAG breakdown into glycerol and FA components
  • Hormonal release in ex stimulates adipose tissue lipolysis, which further augments FFA delivery to active muscle
  • Prolonged ex in fasted/glyc-depleted state places heavy demands on FFA met and enhances fat use as ex energy substrate
27
Q

Ex training and fat met

A
  • Regular aerobic ex profoundly improves ability to ox long-chain FAs, particularly from TAG stored within active muscle, during mild  moderate intensity ex
  • Greater uptake by trained limb during moderate ex through 6 mechanisms
28
Q

increased acetyl-CoA will inhibit what?

A

pyruvate dehydrogenase complex

29
Q

what will inhibition of PRK do?

A

inhibit carbohydrate oxidation and glycolysis

30
Q

what is FA transport across cell membranes dependant on?

A

plasma fatty acid concentration

31
Q

functional carriers used in FA transport

A

Fatty acid binding protein (FABP)

Fatty acid translocase (FAT/CD36)

Fatty acid transport protein (FATP)

ESS1606 Nutrition and metabolism (19 decks)

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