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Metabolism > Fatty Acid Oxidation > Flashcards

Fatty Acid Oxidation Flashcards

1
Q

Two different types of nutritional status

A

Fed state- blood substrate excess

Fasted state- blood substrate deficiency

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2
Q

How does metabolism in distant tissues respond to changes in blood substrate concentration?

A

Taking substrate from blood into tissue
Returning substrate from tissue to blood
Diverting substrate within tissue into energy generating pathways

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3
Q

3 major hormones influencing metabolism + how they work

A

Insulin
Secreted by beta cells of the pancreas in the fed state
Stimulated by increasing blood glucose, certain amino acids and certain fatty acids
Signal of substrate excess/fed state
Tells tissues to store fuel and breakdown glucose

Glucagon
Secreted by alpha cells of the pancreas in the fasted state
Stimulated by low blood glucose
Signal of substrate deficiency/fasted state
Only acts on liver
Signal to liberate glucose from liver to fuel other tissues

Adrenaline
Secreted by the adrenal gland
Fight or flight response
Tell tissues to divert substrates towards making ATP

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4
Q

Functions of lipids

A

Source of energy NEFA and TAG
Large stores of energy, more energy per molecule than glucose
Rapidly mobilised and stored
Ideal for tissues with a high energy demand
Can’t be used by brain or red blood cells
Requires more oxygen to extract the energy than glucose
Make ketone bodies during fasting
Stored in adipose tissue for later use

Structural role- cholesterol, phospholipids
Signalling role- phospholipids, prostaglandins, steroid hormones

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5
Q

2 different sources of fats

A

Dietary fats from digestive tract

Synthesised fats made in liver, de novo synthesis

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6
Q

How are the lipids digested in the intestine?

A

Large triglyceride droplets, hydrophobic and inaccessible

Add bile salts, powerful detergents that break down into smaller droplets

Can now be attacked by pancreatic lipases, as they require a large surface area to volume ratio to operate

Lipases break down TAGs, generating NEFA and glycerol which makes mixed micelles with a hydrophobic centre and hydrophilic surface which can now be absorbed into intestinal wall

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7
Q

NEFA definition

A

non esterified fatty acids- fatty acids that are free

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8
Q

TAG definition

A

triglycerides- 3 fatty acids with a glycerol back bone

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9
Q

stages of chylomicron packaging

A
  1. triglycerides are emulsified by bile and hydrolysed by lipase to form a mixture of fatty acids and monoglycerises
  2. these pass into the enterocyte from the interstitial lumen, where they resterify to form triglycerides
  3. the triglycerides are then combined with phospholipids, cholesterol and apolipoprotein B-48 to form a nascent polypeptide
  4. these are then released by exocytosis from the enterocytes into the lacteals, lymphatic vessels originating in the villi of the small intestine
  5. then secreted into the bloodstream at the thoracic duct’s connection with the left subclavian vein
  6. within the blood, chylomicrons exchange components with HDL, forming a mature chylomicron
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10
Q

important enzyme + function

A

lipoprotein lipase
-sits on the surface of endothelial cells

hydrolyses tag in chylomicron into NEFA

this releases NEFA for uptake by adipose and muscle

LPL is upregulated by insulin

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11
Q

what can + can’t move across the membrane?

A

can- NEFA

cannot- tags, chylomicrons

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12
Q

how are NEFAs transported + why?

A

transported in blood where they are bound to albumin, as NEFA are not water soluble

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13
Q

lipolysis definition

A

process by which fats are broken down in our bodies through enzymes and water or hydrolysis, taking place in adipose tissue

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14
Q

what enzyme regulates lipolysis?

A

hormone-sensitive lipase

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15
Q

hormone-sensitive lipase function

A

hydrolyses TAG into 3 fatty acids and glycerol

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16
Q

how + when is HSL turned on?

A

during starvation

adrenaline binds to receptors to stimulate cAMP pathway, activating PKA

phosphorylates HSL, so becomes functional

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17
Q

how + when is HSL turned off?

A

during fed state, stimulated by insulin

insulin activates protein phosphatase, which leads to the dephosphorylation of HSL

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18
Q

What molecules regulate lipolysis?

A

insulin

  • lack of insulin tells HSL to speed up lipid glycolysis + break down to produce more ATP
  • increased fatty acid levels at night

adrenaline- released during prolonged exercise/ periods of stress

19
Q

Why is glucagon not important in regulation?

A

no glucagon release during fasting, as it only acts on liver not adipose

20
Q

Plasma NEFA with different hormones

A

insulin- 0.3-0.6 mmol/L

adrenaline - 0.8-2 mmol/L

fasting- glucagon- 0.5-2 mmol/L

thyroxine- 0.6-0.8 mmol/L

21
Q

What is stored in non adipose tissue?

A

small quantities of TAGs which will provide a source of energy to suddenly increase oxidative phosphorylation

22
Q

Why must the concentrations be small?

A

adipose is adapted to contain large quantities of fat, however other tissues are not

TAG stores must be kept low to prevent compromising cell function

if too much tag is put into non adipose tissue steatosis occurs such as non alcoholic fatty liver disease, cardiac lipotoxicity in type 2 diabetes

23
Q

important features of fatty acid metabolism in the heart

A

60-70% of ATP in the heart comes from oxidation of fatty acids supplied as NEFA-albumin or a CM/VLDL- TAG

if external fatty acid supply is insufficient, the heart will metabolise endogenous intracellular TAG reserves

fats are more energy rich than carbohydrates

the heart needs more ATP than any other organ

leaves glucose for organs that must use it

24
Q

important features of fatty acid metabolism in the kidneys

A

kidneys need a large amount of energy to accomplish reabsorption

kidneys consume 10% of oxygen used in cellular respiration

renal medulla has poor oxygen supply so there is limited mitochondrial respiration, more anaerobic pathways

25
Q

different types of skeletal muscle

A

type I - slow twitch, oxidative fibres

type II- fast twitch, glycolytic fibres

type IIA- slower fast twitch

type IIB- faster fast twitch

26
Q

what determines distribution of fibres?

A

most muscle fibres will be made up of all three

relative contributions of each will be determined by genetics, activity levels and activity type

27
Q

4 stages of NEFA metabolism

A

uptake, activation, carnitine shuttle, beta oxidation

28
Q

what are the two mechanisms for fatty acid uptake?

A

diffusion across the membrane via a flip flop mechanism

transporter mediated uptake

29
Q

explain transporter mediated uptake + what it allows for

A

fatty acid translocase FAT/CD36 is the primary transporter in oxidative tissues regulating uptake

transporter dependent process allows for control

30
Q

What happens to the NEFAs once in the cell + why?

A

bind to cytoplasmic Fatty Acid Binding Protein- cFABP, as the fatty acids in the cytosol are insoluble

performs a similar role to albumin

31
Q

Explain the activation of fatty acids

A

Co-enzyme A molecule is added to their structure to produce fatty acid coenzyme A, with the addition of ATP and release of AMP and PPi

catalysed by Acyl-CoA Synthetase

32
Q

what problem does the fatty acyl CoA then encounter?

A

needs to get inside the mitochondria to become oxidised, however the inner membrane is highly impermeable

there are no specific transporters for fatty acyl CoA

33
Q

What is the solution called?

A

the carnitine shuttle

34
Q

stages of the carnitine shuttle

A
  1. fatty acyl CoA diffuses across the outer membrane into the inter membrane space
  2. fatty acyl CoA is combined with carnitine and catalysed by carnitine palmitoyl transferase CPT 1 which forms fatty acyl carnitine
  3. fatty acyl carnitine then moves through the inner membrane via the carnitine acyl translocase CAT membrane transporter
  4. the fatty acyl carnitine is then recombined with CoA to form fatty acyl CoA and carnitine, catalysed by CPT 2
35
Q

How is the carnitine concentration maintained in the inter membrane space?

A

CAT is an anti porter, so for every fatty acyl carnitine moved out a carnitine is moved in

36
Q

beta oxidation cycle stages

A
  1. fatty acyl CoA to trans enoyl CoA, FAD to FADH2 catalysed by acyl CoA dehydrogenase in an oxidation reaction
  2. trans enoyl CoA with H2O to form hydroxyacyl CoA, hydration reaction catalysed by enoyl CoA hydratase
  3. hydroxyacyl CoA oxidised to ketoacyl CoA, NAD to NADH catalysed by hydroxyacyl CoA dehydrogenase
  4. ketoacyl CoA and CoASH to form fatty acyl CoA and acetylCoA catalysed to ketoacyl CoA thiolase in a thiolysis reaction
37
Q

What is different about the terminal fatty acyl CoA?

A

It has two less carbons

38
Q

How does the acyl CoA dehydrogenase vary? + why?

A

VLCAD- very long chain

LCAD- long chain

MCAD- medium chain

SCAD- short chain

able to utilise all lengths of fatty acid to ensure maximum activity

39
Q

products of beta oxidation

A

multiple FADH2

multiple NADH + H+

multiple acetyl CoA units

40
Q

where does the acetyl CoA then feed in?

A

Krebs cycle

41
Q

2 Sites at which fatty acid oxidation is regulated

A

hormone sensitive lipase

carnitine shuttle

42
Q

explain hormone sensitive lipase regulation

A

a lot of glucose, insulin is secreted

insulin activates protein phosphatase

dephosphorylates hormone sensitive lipase, so does not convert TAG to NEFAs

43
Q

explain carnitine shuttle regulation

A

during lipogenesis, acetyl CoA forms palmitate

Malonyl CoA is an intermediate in this pathway

malonyl CoA allosterically inhibits CPT 1

this prevents breaking down the lipids that are being made by the body

44
Q

defects in fatty acid oxidation

A

systemic carnitine deficiency

  • rare genetic disorder that presents with cardiomyopathy, fatty infiltration of organs and muscle weakness
  • defect in CPT 2

Jamaican vomiting sickness

  • poisoning of an enzyme
  • ackee contain hypoglycin A which when metabolised inhibits acyl CoA dehydrogenase, preventing beta oxidation
  • body can only use glucose, hypoglycaemia, coma and death

Metabolism (13 decks)

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