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Exercise Biochemistry > Lipid metabolism > Flashcards

Lipid metabolism Flashcards

1
Q

How much energy does 1g of fat provide?

A

9kcal (39kJ)

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2
Q

How much energy is stored as triacylglycerols in a lean individual?

A

3000,000 kJ

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3
Q

Why is fat vital?

A

Adipose tissue protects vital organs, insulates us from cold and gives our bodies & faces their shape

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4
Q

How much fat can we store?

A

Unlike glycogen, where the amount is limited, we can theoretically store an infinite amount of fat – and in evolutionary terms , it will have been in our best interest to be efficient storers of energy

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5
Q

What are the main roles of lipids?

A

-Constituents of membranes (Cholesterol, phospholipids, sphingolipids and glycolipids)

-Sources of metabolic energy
(Triacylglycerols (storage), fatty acids
and ketone bodies)

-Hormones
(Steroids and eicosanoids)

-Other
(Bile salts and waxes)

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6
Q

What are the two types of fats?

A

Saturated or unsaturated

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7
Q

What are essential fatty acids

A

They are fats that we cannot make in the body and are usually PUFAs – that are precursors for important signalling molecules – prostaglandins, thromboxanes

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8
Q

What is the main function of a triacylglycerol?

A

Main storage from of lipids in humans

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9
Q

What is the main function of a phospholipidsl?

A

Major component of cell membranes

Examples include:

phosphatidyl cholines

phosphatidyl inositols

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10
Q

How are triaclglycerols synthesised?

A

Fatty acids activated by attachment to Coenzyme A (CoA)

Fatty acids are added to glycerol-3-P by glycerol phosphate acyltransferase

Removal of phosphate group by a phosphatase before final fatty acid addition

Either synthesised from glycerol or from dihyroxyacetone

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11
Q

What are the enzymes responsible for lipolysis?

A

1 – desnutrin (ATGL) + hormone sensitive lipase (HSL)

2 – HSL

3 – HSL + monoacylglycerol lipase

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12
Q

What is the process of lipolysis?

A

Triacylglycerol –> Diacylglycerol –> Monoacylglycerol –> Glycerol

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13
Q

Where are Triacylglycerols stored?

A

Triacylglycerols stored in fat cells (adipose tissue) and in skeletal muscle

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14
Q

Where does Triacylglycerol synthesis and breakdown occur?

A

In the cytosol

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15
Q

When does lipolysis occur?

A

Starvation, cold and exercise

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16
Q

What hormone controls lipolysis?

A

hormone-sensitive lipase

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17
Q

What hormones increase lipolysis and which reduce?

A

INCREASE
Adrenalin, noradrenalin (via β-adrenergic receptors), glucagon & growth hormone

DECREASE
Adrenalin, noradrenalin (via α2-adrenergic receptors), & insulin reduce lipolysis

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18
Q

What is the difference in lipolysis control in the muscle?

A

in muscle, control of HSL is different – AMPK is the prime controlling mechanism

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19
Q

Go through the regulation of adipose triacylglycerol metabolism

A

GPCR1 = beta adrenergic receptor, GPCR2 = alpha 2 adrenergic receptor

Stimulatory and inhibitory G – protein coupled receptor (GPCRs) modulate cAMP levels. Insulin receptor binding decreases cAMP levels by increasing activity of phosphodiesterase.
Hormone bind to the receptors which activate g proteins which activate an enzyme that converts ATP to cyclic AMP. This causes another few steps until protein kinase A is activated and therefore hormone sensitive lipase.

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20
Q

What are perilipins?

A

They are in adipose tissue and also regulate lipolysis. Under basal conditions they prevent lipolysis but under stimulation by catecholamines perilipin allows lipolysis.

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21
Q

How do perilipins work?

A

ATGL (desnutrin) and HSL are physically prevented from binding to the lipid droplet by the perilipin which surrounds it. Once phosphorylated by PKA, the perilipin is no longer able to block access of desnutrin and activated HSL (note that phosphorylation activated HSL, but inactivates perilipin, allowing increased lipolysis

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22
Q

How is hormone sensitive lipase regulation different in muscle during exercise?

A

HSL is activated by protein kinase A via adrenalin binding to β-adrenergic receptors

Elevated calcium levels activate other protein kinases e.g. protein kinase C

Raised AMP levels also activate AMP-activated kinase (AMPK) – this is the main regulator of HSL phosphorylation in active muscle

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23
Q

How does training chnage activation of desnutin?

A

Training increases the activation of desnutrin in muscle

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24
Q

What are the problems with fats?

A

Triacylglycerols and fatty acids are very hydrophobic – INSOLUBLE in aqueous environments

They need to be transported round the body in association with proteins (LIPOPROTEINS/ALBUMIN)

Transporters are also needed to transport fatty acids effectively across cellular and organelle membranes in addition to diffusion (Fatty acid binding proteins and translocases)

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25
Q

What happens to fatty acid transporter proteins in muscle after endurance and high intensity training?

A

Endurance and high intensity interval training increase levels of fatty acid transporter proteins in muscle – enhancing efficiency of fatty acid utilisation during exercise

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26
Q

What is the function of Chylomicrons?

A

deliver triacylglycerols to the muscles and adipose tissue from the intestine via circulation system.

27
Q

What is the function of VLDL?

A

form IDLs and LDLs as TAG is removed

28
Q

What is the function of IDL?

A

transfer lipids to liver forming LDLs which are enriched in cholesterol.

29
Q

What is the function of LDL?

A

deliver cholesterol from liver to other

cells. (“bad” cholesterol).

30
Q

What is the function of HDL?

A

transport cholesterol from tissues to the liver. (opposite function to LDL). Lipid-depleted HDL then re-enters the circulation. (“good” cholesterol).

31
Q

How do fatty acids arrive at peripheral tissue?

A
  • in chylomicrons or VLDL released by lipoprotein lipase

- from adipose tissue fatty acids transported to tissues bound to albumin

32
Q

how are fatty acids activated for oxidation for energy?

A

They are then activated by attachment to CoA and oxidised in a 4 step repeated pathway to produce acetyl CoA

33
Q

Why can’t the brain oxidise fatty acids?

A

The fats cannot cross the blood brain barrier

34
Q

What is the overall reaction to from acetyl coA from fatty acids?

A

fatty acid + ATP + CoA –> acyl-CoA + PPi + AMP

35
Q

How is acetyl coA transported from the cytosol to the mitochondria?

A

by carnitine

36
Q

What enzymes are used to create carnitine and so move aceltycoA across the blood brain barrier?

A

1- carnitine palmitoyl transferase I

2-Carnitine palmitoyltransferase II

37
Q

What are the 4 steps of Fatty acid oxidation in the mitochondrion?
Fatty acyl-CoA –> acetyl CoA

A
  1. Oxidation by flavoenzyme acyl-CoA dehydrogenase (AD) –> C=C (trans)
  2. Hydration of C=C by enoyl-CoA hydratase (EH) –> 3-L-hydroxyacyl-CoA
  3. Oxidation by 3-L-hydroxyacyl-CoA (HAD) –> β-ketoacyl-CoA
  4. C-C cleavage by CoASH (catalyst β-ketoacyl-CoA thiolase (KT) –> fatty acyl-CoA (2C shorter) and acetyl CoA
38
Q

What does fatty acid oxidation produce?

A

Fatty acid oxidation produces NADH & FADH2 which feed electrons into the electron transport chain for ATP synthesis, and acetyl CoA which feeds into the Krebs Cycle

39
Q

How is fatty acid oxidation different to glycolysis?

A

Unlike glycolysis, no ATP formed directly – NO energy can be formed from fats in anaerobic conditions

40
Q

What is the difference in overall ATP produced from fatty acids to glucose?

A

Overall reaction produces 108 ATP from each molecule of palmitoyl CoA (compare 30-32 from a molecule of glucose)

41
Q

What is the difference in oxidation in unsaturated and saturated fatty acids?

A

Unsaturated fatty acids require additional steps to converts cis double bonds to trans form

42
Q

How is the rate of fatty acid oxidation regulated?

A

Fatty acid oxidation in largely regulated by access of fatty acids to the mitochondria – this is controlled by the concentration of malonyl CoA

43
Q

How does malonyl CoA inhibit fatty acid oxidation?

A

Malonyl CoA is formed by acetyl CoA carboxylase - first step of fatty acid synthesis

High [malonyl CoA] inhibits carnitine acyl-transferase-1

This ensures that fatty acid breakdown is inhibited when energy is plentiful

44
Q

How are ketone bodies formed?

A

Ketone bodies are formed from excess acetyl CoA

45
Q

When does ketone synthesis occur?

A

Synthesis occurs in the mitochondria of liver cells under conditions where the body relies on fatty acid oxidation for energy
fasting/v low CHO diets
uncontrolled diabetes

Ketone bodies are released into the blood and are oxidised to produce energy in peripheral tissues including brain tissue

46
Q

What can high ketone body levels lead to?

A

ketoacidosis

47
Q

Why do starving/fasting individuals synthesise ketones?

A

Low carbohydrate intake – insulin low, glucagon high

Glycolysis is inhibited, [pyruvate] low

Gluconeogenesis is NOT inhibited – oxaloacetate & malate being removed to form glucose

In the absence of insulin, fatty acids are mobilised from adipose tissue and oxidised to acetyl CoA – acetyl CoA levels HIGH

But lack of oxaloacetate prevents acetyl CoA from entering the Krebs cycle

So ketones are synthesised instead

48
Q

Where does fatty acid synthesis occur?

A
  • mainly in the liver in the cell cytoplasm
  • in adipose tissue
  • in breast tissue during lactation
49
Q

As Acetyl CoA cannot cross the inner mitochondrial membrane what happens?

A

Acetyl CoA binds with oxaloacetete to form citrate which moves into the cytosol where acetylCoA is released and oxoacetete reformed.

NADH then binds too oxaloacetete to form malate, NADPH is then released and pyruvate is formed which then goes back to the mitochondria were it is converted to oxaloacetete and the cycle can continue

50
Q

How many complex sites are there on the Fatty acid synthase complex (FAS)?

A

7

51
Q

How many steps are there in fatty acid synthesis?

A

4

Two reduction steps and one dehydration step

52
Q

What is the initial product of fatty acid synthesis?

A

Palmitate

53
Q

What controls the rate of fatty acid synthesis?

A

Acetyl CoA carboxylase

54
Q

What affects the activity of Acetyl CoA carboxylase?

A

Phosphorylation affects activity of Acetyl CoA carboxylase -

phosphorylation, glucagon and high [AMP] (low energy level) inactivates enzyme

activated by high [citrate] (signals high acetyl CoA) and insulin

55
Q

Where is cholesterol mainly obtained?

A

From the diet – eggs (yolk), liver, meat – i.e. mainly animal sources
Intake from < 50 mg/day (vegetarians) to 750mg/day

Synthesis – in almost all tissues - mainly in the liver and intestine

56
Q

How is cholesterol transported?

A

In LDL

57
Q

Why do we need cholesterol?

A

membranes, Vitamin D, Hormones and bile salts

58
Q

What are the 4 steps of cholesterol biosynthesis?

A
  1. Acetyl CoA to mevalonate (C6)
  2. Mevalonate to phosphorylated isoprene units (C5) (activation)
  3. Polymerise 6 isoprene units to form C30 chain (squalene)
  4. Cyclisation to form ring structure (lanosterol) then cholesterol
59
Q

Where does cholesterol biosynthesis occur?

A

Occurs in cytosol and smooth endoplasmic reticulum

60
Q

What is Familial hypercholesterolaemia?

A

lack of LDL receptors - sufferers are at increased risk of coronary disease

61
Q

What does a high level of LDL increase risk of?

A

atherosclerosis

62
Q

What does HDL do?

A

HDL involved in reverse cholesterol transport returning cholesterol from peripheral cells to liver

63
Q

What is tangier disease?

A

lack of HDL – sufferers are at increased risk of coronary disease

64
Q

What is an atherosclerosis?

A

Atherosclerosis is caused by the build-up of lipids in the walls of blood vessels (coronary artery).
This damages the vessel wall and a plaque forms of cholesterol, cholesterol esters and macrophages, surrounded by muscle cells that may undergo calcification

If the plaque ruptures,
a blood clot can form blocking
the vessel and causing
a heart attack or stroke

Exercise Biochemistry (11 decks)

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