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MIMS: Bioenergetics and metabolism > Oxidation of fat > Flashcards

Oxidation of fat Flashcards

1
Q

How is fat stored

A

Stored as triacylglycerols (also called neutral fats or triglycerides), which are uncharged esters of fatty acids with glycerol.

Storage is in adipocytes and (less healthily) in the liver

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2
Q

What proportion of dietary lipid is in the form of triacylglycerols?

A

90%

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3
Q

What is the advantage of using fats in metabolism?

A

They don’t require hydration

Adipose tissue storage unlimited

They are a highly reduced fuel

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4
Q

What is the function of lipases?

A

Converts triglycerides into glycerol and free fatty acids

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5
Q

What are free fatty acids bound to in transportation?

What is the purpose of this?

A

Albumin

Prevents damage to capillaries

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6
Q

What is the ‘safe’ conc of free fatty acids?

A

2mM

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7
Q

How long would adipose TAG supplies last in starvation?

A

34 days `

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8
Q

What is the function of hormone sensitive lipase?

A

converts TAG to DAG to MAG to FFA

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9
Q

What enzyme(s) converts TAG to DAG?

A

Adipose triglyceride lipase (ATGL) and hormone sensitive lipase (HSL)

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10
Q

What enzyme(s) converts DAG to MAG?

A

HSL

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11
Q

What enzyme(s) converts MAG to FFA?

A

HSL and MAGL

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12
Q

What is DAG?

A

Diacylglyceride

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13
Q

What is MAG?

A

Monoacylglyceride

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14
Q

How is HSL activated?

A

Phosphorylation catalysed by protein kinase A

cAMP raised by a number of hormones
Including glucagon (liver not adipose), adrenaline and noradrenaline
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15
Q

What inhibits HSL?

A

Insulin activates phosphodiesterase to lower cAMP

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16
Q

What raises FFA levels?

A

Fasting, prolonged exercise, stress and strong black coffee

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17
Q

What mediates long term effects of hormonal HSL control?

A

Thyroxine and glucocorticoids

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18
Q

What happens to FFA released from

adipose tissue?

A

Taken up by liver and muscle, where
FFA inhibits glucose utilisation as fuel

Most goes to skeletal muscle and heart during sustained exercise

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19
Q

Where does β-oxidation occur?

A

Inner membrane of the mitochondria

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20
Q

What is β-oxidation?

A

A process whereby aliphatic fat is converted into aceyl CoA which can be used in the Kreb’s cycle

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21
Q

How is FFA prepared for β-ox?

A

Fatty acids cleaved from glycerol backbone activated using CoA to form acyl-CoA via fatty acid synthase

The formation of a high energy bond between CoA-SH and a fatty acid results in ATP being converted to AMP.

The overall reaction is made favourable because the PPi formed is hydrolysed to Pi

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22
Q

Why are there different acyl-CoA synthases?

A

For different chain-length fatty acids

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23
Q

What is the role of carnitine in β-ox?

A

Activation occurs at the outer mitochondrial membrane but the resulting fatty acyl-CoA cannot diffuse across the membrane

Carnitine transports fatty acid after modification by carnitine acyl-transferase I

Once inside the fatty acid is transferred back to CoASH in a reaction catalysed by carnitine acyltransferase II

24
Q

What happens in the first oxidative stage of β-ox?

A

An activated fatty acid is oxidized to introduce a double bond

25
Q

What happens in the hydration stage of β-ox?

A

The double bond is hydrated (addition of water) to introduce an oxygen

26
Q

What happens in the second oxidative stage of β-ox?

A

The alcohol group is oxidized to a ketone

27
Q

What happens in the thiolysis stage of β-ox?

A

Coenzyme A attacks at Cβ to yield acetyl-CoA and a fatty acid chain two carbons shorter

28
Q

How is β-ox initiated in monounsaturated fats?

A

There is an isomerase which shifts the double bond so that it is on the normal oxidation pathway.

29
Q

How is β-ox initiated in polyunsaturated fats?

A

One double bond is shifted in the same way and others are reduced to form standard saturated bonds

30
Q

What is the purpose of β-oxidation

A

FADH2, NADH, and acetyl-CoA are all generated

Thus, we can generate ATP by oxidation in the citric acid cycle (for acetyl-CoA) and oxidative phosphorylation (for all the NADH and FADH2 generated)

31
Q

How many reaction cycles are required for the degradation of palmitoyl CoA (C16-acyl CoA)

A

7

32
Q

What is the stoichiometry of oxidation of palmitoyl CoA?

A

Palmitoyl-CoA + 7FAD + 7NAD+ + 7CoA + 7H2O ——> 8acetyl-CoA + 7FADH2 + 7NADH + 7H+

33
Q

How much ATP is generated from the degradation of palmitoyl CoA?

A

106

7NADH

7FADH2

8 acetyl CoA (each citric acid yields 10)

2 ATP used in activation of palmitate

34
Q

What does the fetal heart metabolism rely on?

When are fatty acids first used in metabolism?

A

Glucose

After birth

35
Q

How many FAD-dependent acyl-CoA dehydrogenases are there?

A

4

36
Q

What are the FAD-dependent acyl-CoA dehydrogenases?

A
  1. Very Long chain acyl CoA dehydrogenase or VLCDH (C12-C24)
  2. Long-chain or LCDH (C8-C20)
  3. Medium chain or MCDH (C4-C12)
  4. Short chain or SCAD (C4-C6)
37
Q

What is MCAD deficiency?

A

Babies cannot oxidise fatty acids so readily, and die during the night when glycogen is depleted

38
Q

What proportion of cot death is due to MCAD deficiency?

A

10%

39
Q

What type of fruit produces sickness due to its role in β-ox?

A

Unripe ackee fruit causes Jamaican vomiting sickness

Contains inhibitor of acyl-CoA dehydrogenases which depletes glycogen reserves

40
Q

What happens to most acetyl CoA in the liver?

A

Not oxidised, instead it is converted into ketone bodies and exported for use by muscle (especially heart) and brain

41
Q

What are the 3 ketone bodies?

A

Acetoacetate

β-hydroxybutyrate

Acetone

42
Q

Which ketone body is exhaled on the breath?

A

Acetone

43
Q

What is meant by ‘fats burn in the flame of carbohydrates’

A

Fatty acid oxidation is incomplete if citric acid cycle intermediates are being drained to make glucose

44
Q

What enzyme to statins target?

A

HMG-CoA reductase in the cytosol to block cholesterol biosynthesis

45
Q

What is HMG-CoA?

A

Liver precursor for de novo synthesis of cholesterol

46
Q

Why does the brain use ketone bodies rather than FFAs when glucose is low?

A

Ketone bodies can cross the blood-brain barrier (unlike FFA )

Soluble, don’t need albumin for transport

47
Q

Can glucose be produced from fat?

What is the exception to this?

A

No

Glycerol produced from TAGs can be recycled. Since adipose tissue does not have glycerol kinase the glycerol must be circulated to the liver

48
Q

What are the 4 mechanisms for the regulation of b-oxidation?

A
  1. Lipolysis of TAG
  2. Re-esterification of fatty acids
  3. Transport into mitochondria
  4. Availability of NAD+ and FAD
49
Q

How is fatty oxidation regulated by re-esterification

A

GPATs (re-esterification enzymes) are inhibited by cAMP-PKA phosphorylation/stimulated by insulin

During fasting the concentration of insulin is low

GluT4 is not recruited in adipose cells
Little glucose uptake
and Glycerol 3-phosphate is low

These changes prevent free fatty acids (as CoA
derivs) from re-esterification

Fatty acids are released to circulate to other tissues

50
Q

How is fatty oxidation regulated by transport into mitochondria?

A

The carnitine shuttle is inhibited at CAT-I by malonyl-CoA in liver

Malonyl-CoA is produced during fatty acid synthesis

Prevents synthesis and degradation occurring alongside each other in liver

51
Q

Where in the body does malonyl CoA act as a regulatory molecule?

A

Liver and muscle

52
Q

How is fatty oxidation regulated by the availability of NAD+ and FAD?

A

There is competition with the citric acid cycle for these co-factors, which can limit activity

53
Q

What is the function of peroxisomes?

A

Mitochondria cannot import very long chain fatty acids (>22 carbons)

Long fatty acids are oxidised in peroxisomes which chew up fats for synthesis purposes and to supply the mitochondria with shorter chain fatty acids

54
Q

How can PPARs be used for treating type II diabetes and obesity

A

PPARα in the liver promotes transcription of genes for FFA use, target for fibrate drugs against hypertriglyceridaemia (risk of coronary heart disease)

PPARγ controls adipogenesis, improves insulin sensitivity, target for thiazolidinediones

PPARδ (or β/δ) is expressed ubiquitously, its activation may combat multiple components of the metabolic syndrome

55
Q

What are PPARs?

A

Peroxisomal Proliferation Activated Receptors

Ligand inducible transcription factors which
regulate energy metabolism by acting as nutritional sensors

Their natural ligands are lipids or lipid-related (but largely unidentified)

MIMS: Bioenergetics and metabolism (4 decks)

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