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Nutrition (Y2S2) > Fat Metabolism > Flashcards

Fat Metabolism Flashcards

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1
Q

What are the two main forms of fat relevant to metabolism?

A

Fatty acid – long hydrocarbon chain + carboxyl group

Triacylglycerol (TAG) – 3 fatty acids bound to a glycerol backbone (main storage form of fat)

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2
Q

What are the types of dietary fats?

A

Saturated fats

Unsaturated fats:
 – Monounsaturated
 – Polyunsaturated

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3
Q

Where in the body is fat stored or found?

A
  • Plasma FFA – free fatty acids in blood (small amounts)
  • Plasma TAGs – in lipoproteins like HDL/LDL (relatively low amounts)
  • Adipose tissue – major fat store
  • IMTG (Intramuscular TAGs) – important energy source in muscle
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4
Q

In what form is all the energy we want to utilise stored in?

A

IMTG and adipose tissue

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5
Q

Where are lipid droplets located within muscle fibres?

A

Intermyofibrillar – between myofibrils
Beneath the sarcolemma (muscle membrane)

  • Always near mitochondria
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6
Q

What surrounds lipid droplets in muscle cells?

A

A single phospholipid layer that keeps triglycerides intact and stable within the cell

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7
Q

What is the role and structure of an adipocyte?

A

Specialised fat storage cell

  • Dominated by a large lipid droplet that takes up nearly the entire cell
  • Very little room for other organelles → storage is its primary function
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8
Q

What are the three stages required to access fat stores in adipose or muscle tissue?

A
  1. Lipid mobilisation
  2. Fatty acid activation
  3. Fatty acid oxidation
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9
Q

What is the structure and function of GPCRs (G-protein coupled receptors)?

A

GPCRs are 7-pass transmembrane receptors

  • Binding of a signal molecule (e.g. adrenaline) causes a conformational change in GPCR = binding of a G-protein
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10
Q

What is G-protein formed of + what is it bound to?

A

3 subunits - alpha, beta and gamma units making it heterotrimeric

  • it is GDP bound (in inactive active)
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11
Q

What happens to the G-protein when a GPCR is activated?

A

The GPCR acts as a GEF (guanosine exchange factor), swapping GDP for GTP

  • G-protein then causes α-subunit to dissociate from the βγ-subunits, activating downstream signalling
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12
Q

What is the role of adenylate cyclase in fat mobilisation?

A

Activated G-protein (Gαs) binds to adenylate cyclase

  • Converts ATP → cAMP + PPi, which acts as a second messenger for intracellular signalling
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13
Q

What is the role of a secondary messenger?

A

Transfer and amplify an extra cellular signal inside the cell

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14
Q

How is cAMP different to AMP?

A

Forms a ring structure so different function (but are very similar)

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15
Q

What is the function of cAMP in fat metabolism?

A

cAMP binds to Protein Kinase A (PKA) enabling catalytic subunits to be active…

PKA phosphorylates key enzymes involved in lipolysis:

 1. Hormone-sensitive lipase (HSL)
 2. Adipose triglyceride lipase (ATGL)
 3. Perilipin (PLIN) proteins

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16
Q

What role do perilipin (PLIN) proteins play in lipid mobilisation?

A

Under resting conditions, PLIN are bound to ABHD5, blocking lipolysis

Phosphorylation of PLIN releases ABHD5 to bind ATGL and initiate lipolysis

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17
Q

How is hormone-sensitive lipase (HSL) activated and what does it do?

A

HSL is phosphorylated by PKA

Moves to the lipid droplet, binds PLIN proteins, and stimulates lipolysis

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18
Q

What enzyme can reverse lipolysis by re-esterifying fatty acids?

A

DGAT – re-esterifies liberated fatty acids back into triglycerides

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19
Q

What are the three enzymatic steps of lipolysis starting from triacylglycerol (TAG)?

A
  1. TAG → DAG + FA by ATGL
  2. DAG → MAG + FA by HSL
  3. MAG → FA + Glycerol by Monoacyl Glycerol Lipase
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20
Q

Why do fatty acids need to bind to albumin in the blood once liberated?

A

Fatty acids are not soluble in aqueous solutions like blood, so they bind to albumin for transport

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21
Q

What happens to the glycerol released during lipolysis?

A

It enters the blood, goes to the liver, and is converted to Glyceraldehyde 3-phosphate, which can:

  • Enter glycolysis as an intermediate
  • Undergo gluconeogenesis
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22
Q

SO how can we tell lipolysis is switched on using one basic marker?

A

Glycerol levels will increase

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23
Q

How do fatty acids enter the muscle cell from the blood?

A
  1. Released from albumin
  2. Transported into the cell via CD36/FAT transporter
  3. Then bound by FABP-PM (plasma membrane) and FABP-C (cytosol) for internal transport
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24
Q

What is fatty acid activation and where does it occur?

A

FA needs to gain entry into mitochondria

  1. Activation = FA reacts with CoA to FA to form Fatty acyl-CoA (makes it more reactive + transferable)
  2. Occurs on the outer mitochondrial membrane (OMM)
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25
Why is carnitine needed for fatty acid oxidation?
Carnitine allows transport of fatty acyl-CoA across the inner mitochondrial membrane, which is otherwise impermeable to fatty acids
26
What is the role of CPT1 in mitochondrial fatty acid entry?
CPT1 is on the outer mitochondrial membrane and transfers carnitine to fatty acyl-CoA, forming acylcarnitine
27
How does acylcarnitine cross the inner mitochondrial membrane (IMM)?
Acyl carnitine moves through Porin in OMM and via acylcarnitine transferase (ACT) on IMM, which works as an anti-porter
28
What enzyme regenerates acyl-CoA inside the mitochondrial matrix?
CPT2 reverses CPT1 reaction + converts acylcarnitine back to acyl-CoA inside the mitochondrial matrix for oxidation
29
What is the role of beta oxidation?
To oxidise the fatty acids (Acyl CoA) via 4 reactions inside the mitochondrial matrix
30
What are the four main reactions involved in beta-oxidation?
- 2 x Oxidation (FAD + NAD are reduced via H+ added) - 1 x Hydration (adding H₂O) - 1 x Thiolysis (HSCoA cleaves 2-carbon unit as Acetyl-CoA) - HS refers to hydrogen bound to sulphur = thiol
31
What is the main products of beta-oxidation + is it just one cycle?
- Acetyl-CoA - FADH₂ - NADH - The Acyl-CoA is shortened by 2 carbons each cycle so the 4 reactions keep occurring until FA is left as a 2 carbon molecule (Acetyl CoA)
32
Where does the Acetyl-CoA produced from beta-oxidation go?
It enters the TCA cycle to produce NADH, FADH₂, and a small amount of ATP
33
Where do NADH and FADH₂ go after the TCA cycle?
They enter the electron transport chain (ETC) to produce ATP - NADH enters at Complex I - FADH₂ enters at Complex II
34
Why are fats considered energy dense?
Fatty acids have long carbon chains (often >22 carbons), storing large amounts of covalent bond energy - Glucose oxidation = ~32 ATP - Fat oxidation = ~106 ATP
35
What happens to fatty acids with an odd number of carbon atoms during beta-oxidation?
They are broken down until Acetyl CoA and a molecule of propionyl-CoA remains, which is then converted to succinyl-CoA and enters the TCA cycle
36
What challenge arises when oxidising unsaturated fatty acids?
Build up of intermediates and cannot proceed through standard beta-oxidation - Isomerases and reductases are needed to convert them into usable intermediates that re-enter beta-oxidation
37
What is ketogenesis?
Most Acetyl CoA enters the TCA cycle, but some is converted to ketone bodies - This occurs when glucose levels are low, such as during fasting
38
Why are ketone bodies useful?
They are water soluble and can be used by some tissues for energy (e.g. brain / heart)
39
What are the main ketone bodies produced, and how are they used?
The main ketone bodies are Acetoacetate and β-hydroxybutyrate - converted back to Acetyl CoA and enter TCA cycle
40
Why are ketone bodies important during fasting?
During fasting, glucose levels are low. - The brain primarily relies on glucose so uses ketone bodies as an alternative energy source
41
What happens to fat oxidation from rest to low/moderate intensity exercise?
Fat oxidation increases significantly—by 5 to 10-fold compared to rest, supplying a large portion of energy (especially up to ~40% Wmax)
42
What are the key hormones that stimulate lipolysis during exercise?
- Adrenaline (via β-adrenoreceptors – GPCRs) - Glucagon (via glucagon receptors – GPCRs) (Both enhance lipolysis; adrenaline is more potent)
43
How does insulin affect lipolysis?
Insulin (from food intake) inhibits lipolysis significantly
44
What is re-esterification?
Re-esterification = reassembly of fatty acids into triacylglycerol
45
How does re-esterification change with exercise?
At rest: ~70% of liberated FAs are re-esterified During moderate exercise: Re-esterification decreases to ~20%, allowing more FAs for oxidation
46
How does tissue blood flow change during low-moderate exercise and why is it important?
Adipose tissue blood flow increases → enhances FA removal Muscle blood flow increases >10-fold → improves FA delivery for oxidation
47
What happens to CD36 content at the muscle membrane during exercise?
CD36 increases at the plasma membrane at the onset of exercise, allowing greater FA uptake from blood into muscle
48
What enzyme facilitates fatty acid entry into mitochondria?
CPT-1 (carnitine palmitoyltransferase 1) converts FA-CoA to Acyl-Carnitine for mitochondrial entry
49
How is CPT1 regulated?
It is allosterically inhibited by malonyl-CoA (conc increases slightly during exercise) - Exercise reduces CPT-1 sensitivity to malonyl-CoA, enhancing fat transport into mitochondria
50
At what exercise intensity is maximal fat oxidation (Fatmax) typically observed?
Around 65% of VO₂max
51
What are the 5 main physiological reasons for increased fat oxidation during low-to-moderate intensity exercise?
1. Increased lipolysis (due to more adrenaline) 2. Decreased re-esterification (more FAs available) 3.Increased blood flow to adipose and muscle tissue 4. Increased CD36 (fatty acid uptake) and CPT1 (mitochondrial transport) 5. Utilisation of intramuscular triglycerides (IMTGs)
52
Does lipolysis decrease at high exercise intensities?
No — lipolysis increases, as indicated by a rise in glycerol concentration, but fatty acid appearance in the blood does not increase - SO lipolysis is increasing but FA's aren't entering the blood
53
Why don’t fatty acids appear in the blood despite increased lipolysis at high exercise intensities?
Reduced blood flow to adipose tissue limits the release of fatty acids into the bloodstream - blood flow shunted towards active musculature
54
What happens to fat oxidation during recovery from high-intensity exercise?
Lipolysis decreases, but FA appearance in the blood increases, suggesting that FA release resumes once blood flow to adipose tissue is restored
55
Can increasing fatty acid availability (e.g. via infusion) enhance fat oxidation at high intensities?
Only slightly — FA infusion increases availability but does not significantly boost fat oxidation at ~85% VO₂max, indicating a muscle-level limitation
56
What does the minimal increase in fat oxidation with FA infusion at high intensities suggest?
That fat oxidation is limited by mechanisms within the muscle, not by FA availability
57
What are four potential muscle-level limitations to fat oxidation at high exercise intensities?
1. Skeletal muscle HSL activity – may be inhibited by AMPK (though unclear) 2. CD36 translocation to plasma membrane – possibly reduced, affecting FA uptake 3. Carnitine content – decreases at high intensities, may limit FA transport (though unclear how much is actually needed) 4. CPT1 activity – may be reduced due to pH or other factors, limiting mitochondrial FA entry
58
How might carnitine influence fat oxidation at high exercise intensities?
Reduced carnitine levels could impair transport of FAs into mitochondria, limiting oxidation
59
What is the Randle Cycle?
The glucose-fatty acid cycle describing how fat metabolism can inhibit carbohydrate metabolism
60
What are the 3 mechanisms of the Randle cycle?
1. High Acetyl CoA inhibits pyruvate dehydrogenase (PDH) activity = important for carb metabolism 2. High citrate can inhibit PFK (rate limiting enzyme in glycolysis) 3. Consequent reduction in glycolytic flux causes build-up of G6P inhibiting hexokinase
61
However, is the Randle Cycle true in humans?
No - it appears mostly untrue
62
In humans, what reduces glycogen phosphorylase activity when fatty acids are elevated?
Reductions in ADP and Pi
63
How can carbohydrate metabolism inhibit fat metabolism (reverse Randle Cycle)?
Increased acetyl CoA from glycolysis (pyruvate) can be converted to malonyl CoA which can inhibit CPT1 and CPT1 can bind to carnitine reducing capacity for FA entry into mitochondria
64
What molecule formed from carbohydrate-derived acetyl CoA inhibits CPT1?
Malonyl CoA
65
What is proposed to compete for TCA cycle entry during high carbohydrate metabolism?
Carbohydrate-derived acetyl CoA competes with fatty acid-derived acetyl CoA
66
Why is carbohydrate a more efficient fuel than fat during intense exercise?
- Carbohydrates produce more ATP per oxygen consumed - Carbs utilise less oxygen for the same amount of ATP
67
Why might skeletal muscle favour carbohydrate metabolism during high intensity exercise?
Faster energy liberation and greater ATP yield per oxygen consumed
68
How does fat oxidation change with exercise duration?
Increases as duration increases due to declining muscle glycogen stores
69
What primarily regulates fat oxidation during exercise?
Carbohydrate availability
70
How does pre-exercise carbohydrate ingestion affect fat metabolism during exercise?
Decreases reliance on fat oxidation
71
Why does carbohydrate ingestion before exercise reduce fat oxidation?
Insulin release from beta cells of pancreas suppresses lipolysis by inhibiting ATGL and HSL
72
Which tissue is most sensitive to insulin’s suppression of lipolysis?
Skeletal muscle
73
What is the relationship between insulin concentration and lipolysis?
As insulin increases, lipolysis suppression increases
74
How does exercise training affect fat metabolism over time?
Increases reliance on fat oxidation
75
What biochemical adaptations support increased fat oxidation with training?
1. Increased CD36 for FA entry in muscle 2. Increased CPT1 for conversion of FA to Acyl Carnitine for mitochondrial entry

Nutrition (Y2S2) (6 decks)

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