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zESA2 > MEH session 4 > Flashcards

MEH session 4 Flashcards

1
Q

Which tissues have an absolute requirement for glucose?

A

Red blood cells
Neutrophils
Innermost cells of kidney medulla
Lens of eye

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2
Q

Some tissues require a continuous supply of glucose. How do they get this?

A

Intermittent availability from the diet
Between meals, stored glucose in glycogen
If period between meals is long enough to deplete stored glycogen (8-12 hours), gluconeogenesis

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3
Q

What should normal plasma glucose concentration be?

A

5mmol/L

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4
Q

Why does blood glucose concentration <0.6mmol/L cause brain damage and eventually death?

A

GLUT 1 transport proteins allow glucose to cross the blood-brain barrier.
The rate of transport of glucose across this protein is dependent on the concentration of glucose in the blood.
At this value, glucose concentration of the blood is below Km for this transporter so there is very little uptake of glucose into the brain.

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5
Q

Where and how is glycogen stored?

A

Stored in granules in

  • the liver (in hepatocytes)
  • skeletal muscle (intramyofibrillar and intermyofibrillar gycogen)
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6
Q

Describe the structure of glycogen.

A

Highly branched polymer of glucose residues - this provides many sites to which glucose residues can be added/removed allowing rapid synthesis or degradation of glycogen

Linked together by alpha 1-4 and alpha 1-6 glycosidic bonds in ratio 10:1

Alpha 1-6 bonds are branch points

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7
Q

What are the advantages of storing glucose as glycogen?

A

Highly branched polymer of glucose residues - this provides many sites to which glucose residues can be added/removed allowing rapid synthesis or degradation of glycogen. Alpha 1-6 bonds are branch points

The large size of the glycogen molecule means that many glucose molecules can be stored with minimal osmotic effect in the storage tissue.

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8
Q

What is required for the synthesis of glycogen?

A

Energy (from ATP and UTP)
Glucose
Water

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9
Q

What is the first step of glycogen synthesis?

A

STEP 1. Hexokinase/Glucokinase

Glucose + ATP —> glucose 6-P + ADP

Same as first step of glycolysis

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10
Q

What is the second step of glycogenesis?

A

STEP 2. Phosphoglucomutase

Glucose 6-P glucose 1-P

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11
Q

What is the third step of glycogenesis?

A

Step 3. G1P uridylylytransferase

Glucose 1-P + UTP + H20 —> UDP-glucose + 2PPi

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12
Q

What is UDP-glucose an intermediate in?

A

Synthesis of many sugar containing molecules (lactose and glycogen)
Interconversion of glucose and galactose.

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13
Q

What is the fourth step of glycogen synthesis?

A

Step 4. Glycogen synthase/Branching enzyme. (IRREVERSIBLE)

Glycogen (n residues) + UDP-glucose —> glycogen (n+1 residues) + UTP

Glycogen synthase links glucose residues in series to a glycogen primer by alpha 1-4 glycosidic bonds.
At appropriate points, branching enzyme links a glucose residue by a alpha 1-6 glycosidic bond introducing a branch point

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14
Q

When is glycogen degraded?

A

Skeletal muscle—> in response to exercise for energy production
Liver —> in response to fasting/part of the stress response released into the blood for use by other tissues

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15
Q

Is glycogen degradation a reversal of the synthetic pathway?

A

No

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16
Q

Which enzyme is involved in both glycogenesis and glycogenolysis?

A

Phosphoglucomutase
Glucose 1-P glucose 6-P

Step 2 of both reactions

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17
Q

What happens to glucose 6-phosphate produced in glycogenolysis in muscle?

A

In muscle, glucose 6-P enters glycolysis and is used to provide energy for the exercising muscle and this can only be used by muscle.

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18
Q

What happens to glucose 6-P produced by glycogenolysis in the liver?

A

In the liver, the glucose 6-P is converted to glucose by the enzyme glucose 6-phosphatase during fasting or stress (this enzyme is absent from muscle)

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19
Q

Which step is irreversible in glycogenolysis?

A

Step 1. Glycogen phosphorylase/Debranching enzyme (IRREVERSIBLE)

Glycogen (n residues) + Pi —> glucose 1-P + glycogen (n-1)

Glycogen phosphorylase breaks the alpha 1-4 bonds. Bonds are subjected to phosphorolysis rather than hydrolysis with the result that glucose residues are released as glucose 1-P rather than free glucose.

Debranching enzyme breaks the alpha 1-6 bonds. This produces free glucose.

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19
Q

Which enzymes are involved in regulation of glycogen metabolism?

A

Controlling the activities of enzymes catalysing irreversible reactions in the biosynthetic and degradative pathways. These enzymes are regulated reciprocally:
Glycogen synthase (STEP 4 of glycogenesis)
Glycogen phosphorylase (STEP 1 of glycogenolysis)
They are regulated by:
Allosteric control
Covalent modification - reversible phosphorylation in response to hormone levels

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20
Q

Which hormones are involved in regulation of glycogen metabolism?

A

1) Glucagon and adrenaline
Inhibit glycogen synthase (via phosphorylation)
Stimulate glycogen phosphorylase (via phosphorylation)

2) Insulin
Stimulates glycogen synthase (via de-phosphorylation)
Inhibits glycogen phosphorylase (via de-phosphorylation)

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21
Q

Glucagon has no effect on glycogen in…

A

Muscle

They do not have glucagon receptors

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22
Q

AMP is an allosteric activator of glycogen phosphorylase in…

A

Muscle but not liver

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23
Q

In Von Glerke’s disease, there is a glucose 6-phosphatase deficiency. How does this present?

A

Hepatomegaly

Enlargement of liver as glucose-6P accumulates

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24
Q

When is glucose produced from non-carbohydrate sources? (Gluconeogenesis)

A

After approximately 8-10 hours of fasting, glycogen sources are depleted. Glucose-dependent tissues require glucose absolutely all the time. Therefore, gluconeogenesis occurs.

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25
Q

Where is the major site of gluconeogenesis?

A

Liver although the kidney cortex can produce glucose during starvation.

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26
Q

What are the possible substrates for gluconeogenesis?

A

1) Pyruvate
2) lactate from anaerobic glycolysis in exercising muscle and red blood cells (Cori cycle)
3) glycerol from adipose tissue and triglycerides
4) Essential and non-essential amino acids whose metabolism involved pyruvate or intermediates of the TCA cycle, mainly alanine
REMEMBER, Acetyl coA cannot be converted to glucose because the reaction catalysed by pyruvate dehydrogenase is irreversible

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27
Q

Which steps of glycolysis are by-passed in gluconeogenesis and how?

A

The irreversible steps of glycolysis:

Step 1 - glucose 6-phoshatase
Step 3 - fructose 1,6 bisphosphate
Step 10 - phosphoenolpyruvate carboxykinase (PEPCK)

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28
Q

Which reaction provides a link between the TCA cycle and gluconeogenesis?

A

By-passing step 10.
It enables the products of amino acid catabolism that are intermediates of the TCA cycle to be used for the synthesis of glucose by being converted directly to oxaloacetate or being converted to pyruvate and then oxaloacetate.

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29
Q

How is gluconeogonesis regulated?

A

Largely under hormonal control as it occurs in response to stress. Importantly the insulin/glucagon ratio. Major control enzymes are:

PEPCK - hormones change the amount of enzyme
Stimulation - glucagon, cortisol
Inhibition - insulin

Fructose 1,6- biphosphatase - hormones change the amount and activity of enzyme
Stimulation - glucagon
Inhibition - insulin

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30
Q

What type of superfamily do insulin receptors belong to?

A

Tyrosine kinase

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31
Q

What type of super family do glucagon receptors belong to?

A

GPCRs

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32
Q

What type of superfamily of receptors do cortisol receptors belong to?

A

Nuclear receptors

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33
Q

How is gluconeogenesis affected in type 1 diabetics?

A

Decreased insulin
Less inhibition of PEPCK and fructose 1,6 biphosphatase
Increased rate of gluconeogenesis
Hyperglycaemia

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34
Q

Why are triacylglycerols an efficient method of storing energy?

A

They can be stored in bulk in an anhydrous form in adipose tissue so do not have an osmotic effect
They are highly calorific
More reduced than carbohydrates so release more energy when oxidised

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35
Q

Where does dietary fat enter the bloodstream?

A

From thoracic duct to left subclavian vein (chylomicrons)

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36
Q

What are the substrates for fatty acid synthesis?

A
  • Acetyl coA (derived from the catabolism of carbohydrate and amino acids- this comes from the mitochondria in combination with oxaloacetate as citrate, the citrate is cleaved in the cytoplasm to release acetyl coA and oxaloacetate)
  • ATP
  • NADPH (from pentose phosphate pathway)
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37
Q

Where and when are fatty acids synthesised?

A

Mainly in the liver- when there is excess glucose. Glucose is the major source of carbon

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38
Q

Which enzymes are involved in fatty acid synthesis?

A

Acetyl coA carboxylase - produces malonyl coA from acetyl coA

Fatty acid synthase complex - builds fatty acids by sequential addition of 2 carbon units provided by malonyl-
CoA.

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39
Q

Is fatty acid synthesis the opposite of beta oxidation of fatty acids?

A

No

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40
Q

How are synthesised triacylglycerols transported in the blood?

A

VLDL

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41
Q

Which enzyme plays an important role in controlling the rate of fatty acid synthesis and how?

A 
Acetyl coA carboxylase - subject to allosteric regulation and covalent modification 
• Allosteric
Activated by:
-citrate 
Inhibited by:
-AMP
• Covalent modification - reversible phosphorylation/dephosphorylation
Activated by dephosphorylation by:
-insulin
Inhibited by phosphorylation by:
-glucagon
-adrenaline
42
Q

Give some differences between fatty acid oxidation and fatty acid synthesis.

A

Oxidation

  • occurs in mitochondria, the enzymes are found in the mitochondrial matrix
  • oxidative - produces NADH and FAD2H
  • requires a small amount of ATP to activate the fatty acid
  • glucagon + adrenaline stimulate
  • insulin inhibits

Synthesis

  • occurs in cytoplasm, fatty acid synthase complex found here
  • reductive - requires NADPH
  • requires a large amount of ATP to drive the process
  • glucagon + adrenaline inhibit
  • insulin stimulates
43
Q

Which enzyme regulates lipolysis?

A

Hormone sensitive lipase

44
Q

What does hormone sensitive lipase do?

A

Converts TAGs to glycerol and free fatty acids

Glycerol —> travels to liver and utilised as carbon source for gluconeogenesis

Free fatty acids —> travels complexed with albumin to muscle and other tissues

45
Q

Which tissue contains the greatest mass of glycogen?

A

Skeletal muscle

46
Q

Which effect would the hormone glucagon have on the enzyme glycogen synthase in the liver?

A

Decrease in activity

47
Q

Which effect would the hormone insulin have on the enzyme glycogen phosphorylase in muscle?

A

Decrease in activity

Glycogen phosphorylase is the rate limiting enzyme in glycogen degradation

48
Q

Which are the two major control enzymes for gluconeogenesis?

A

PEPCK

Fructose 1,6-biphosphatase

49
Q

Which effect would the hormone insulin have on the enzyme hormone sensitive lipase?

A

Decrease in activity

Hormone sensitive lipase breaks down triacylglycerol into fatty acids and glycerol

50
Q

Lipids are insoluble in water so how are they found in the plasma?

A

In association with protein.
Most of the lipid (approximately 98%) is carried as highly specialised non-covalent assemblies known as lipoprotein particles. These have usually come from the diet or are synthesised in the body and are being transported to tissues for storage/utilisation.
The remaining 2% (mostly fatty acids) is carried bound non-covalently to albumin. These albumin bound fatty acids are fatty acids released from adipose tissue during lipolysis and are used as a fuel by tissues such as muscle.

51
Q

What different types of lipids are found in the blood?

A

Triacylglycerol
Phospholipids
Cholesterol
Free fatty acids

52
Q

What should total plasma cholesterol be?

A

<5mmol/L

53
Q

Describe the structure of a phospholipid

A 
Hydrophilic head 
Glycerol 
Phosphate 
Head group (classified by their head group eg. 
Choline---> phosphatidylcholine, 
inositol--->phosphadylinositol)

Hydrophobic tail
2 fatty acids (saturated or unsaturated)

54
Q

How can phospholipids be arranged?

A

Bilayer sheet - bilayer with hydrophilic heads pointing outwards and hydrophilic tails pointing inwards
Liposome - bilayer phospholipid sphere with hydrophilic centre and hydrophilic surface
Micelle - single layer phospholipid sphere with hydrophobic centre and hydrophilic surface

55
Q

How are phospholipids in plasma lipoproteins arranged?

A

Micelle- single layer of phospholipid with hydrophilic heads pointing out of the sphere and hydrophobic heads pointing inwards

56
Q

Where does most of our cholesterol come form?

A

Some cholesterol is obtained from our diet

However, most is synthesised in the liver

57
Q

What is cholesterol used for?

A 
Precursor of steroid hormones:
Cortisol
Aldosterone
Testosterone
Oestrogen

Precursor of bile acids

58
Q

How is cholesterol transported around the body?

A

As cholesterol esters (cholesterol wit a fatty acid chain)

They are esterified with a fatty acid by either the enzyme LCAT or acetyltransferase

59
Q

What are plasma lipoproteins composed of?

A

These are multi-molecular complexes that contain:
• variable amounts of different lipids (phospholipids, cholesterol, triacylglycerols and cholesterol esters) in non-covalent (mostly hydrophobic)
• In association with specific proteins (apoproteins)

60
Q

Describe the structure of a lipoprotein.

A 
• Spherical particles 
• Surface coat (shell)
	◦ Phospholipid monolayer 
	◦ Small amount of cholesterol 
	◦ Peripheral apoproteins eg. ApoC, ApoE
	◦ Integral apoproteins (span the monolayer) eg. ApoA, ApoB
• Hydrophobic core 
	◦ Triacylglycerols
	◦ Cholesterol esters
	◦ Fat soluble vitamins
61
Q

What are the different classes of plasma lipoproteins?

A 
Chylomicrons 
VLDL
IDL
LDL
HDL
62
Q

Which plasma lipoprotein is referred to as ‘good cholesterol’ in Lay terms?

A

HDL

63
Q

Which plasma lipoproteins are the main carriers of triacylglycerol?

A

Chylomicrons

VLDL

64
Q

Which plasma lipoproteins are the main carriers of cholesterol?

A

IDL
LDL
HDL

65
Q

How can the different classes of lipoprotein be separated from one another?

A

Electrophoresis
HDL will travel the furthest
VLDL will travel the least

Or

Ultracentrifugation
HDL at top
VLDL at bottom

66
Q

Order the plasma lipoproteins from smallest to largest

A 
HDL
LDL
IDL
VLDL
Chylomicrons

(Particle diameter inversely proportional to density)

67
Q

Someone who had just eaten had their blood tested for plasma lipoproteins. Which plasma lipoprotein may not be present?

A

Chylomicrons

Only present in blood 4-6 hours after a meal

68
Q

What is the function of apoproteins in lipoproteins?

A

Structural:
Packaging water insoluble lipid

Functional:
Co-factor for enzymes
Ligands for cell surface receptors

69
Q

In which plasma lipoprotein is ApoAI found?

A

HDL

70
Q

Which apoprotein is added to chylomicrons before entering the lymphatic system?

A

ApoB-48

71
Q

Which apoproteins are added to chylomicrons once they are in the blood?

A

Apoc and ApoE

72
Q

What is the function of ApoC in chylomicrons?

A

It binds to lipoprotein lipase on adipocytes and muscle. This hydrolyses the TAGs to release the fatty acids that enter the cell whee they are re-converted to TAGs for storage (adipose) or utilised for energy production (muscle)

73
Q

When triglyceride content is reduced to approximately 20%, what happens?

A

It becomes a chylomicron remnant. These return to the liver. The LDL receptor on hepatocytes bind to ApoE and the chylomicron remnant is taken up by receptor mediated endocytosis. Lysosomes release the remaining contents for use in metabolism.

74
Q

What is the primary function of VLDL?

A

Transport of triacylglycerol synthesised in the liver to adipose tissue for storage

75
Q

How are VLDL particles made?

A
  • ApB100 is added is added during formation

* ApoC and apoE are later added from HDL particles in the blood

76
Q

How and where are VLDL particles metabolised?

A
  • VLDL binds to lipoprotein lipase (LPL) on capillary endothelial cells in muscle and adipose
  • In the muscle, the released fatty acids are taken up and used for energy production
  • In adipose tissue, the fatty acids are used for re-synthesis of triacylglycerols and stored as fat
  • The VLDL starts to become depleted of triacylglycerol
  • Some VLDL particles dissociate from LPL and return to the liver
  • However, if the TAG content in the VLDL further depletes to approximately 30%, the particle becomes a short-lived IDL particle
  • However, if the TAG content in the IDL further depletes to approximately 10%, IDL loses apoC and apoE, and becomes an LDL particle (high cholesterol content).
77
Q

What is the primary function of LDL?

A

Provides cholesterol from the liver to peripheral tissues

78
Q

How do tissues obtain the cholesterol they need?

A

Receptor-mediated endocytosis
In this process, the LDL particles are taken up by the cell and cholesterol is released inside the cell.
• Cells requiring cholesterol synthesise specific LDL receptors that are exposed on the cell surface.
• The LDL receptors recognise and bind to apo B100 on the surface of LDL particles.
• The receptor with its bound LDL particle is taken into the cell by endocytosis and subjected to lysosomal digestion.
• In this process, cholesterol esters are converted to free cholesterol that is released within the cell.
• This cholesterol can be stored (as cholesterol esters) or used by the cell.
• This process inhibits the synthesis of cholesterol by the cell and reduces the synthesis and exposure of LDL receptors.

79
Q

Why are LDL’s not efficiently cleared by the liver?

A

They do not have apo C or apo E

Liver LDL-receptor has a high affinity for apoE

Therefore, they have a relatively long half life

80
Q

Why is the relatively long half life of LDL particles clinically relevant?

A

The half-life of LDL particles in blood is much longer than VLDL or IDL particles since they are not efficiently cleared by the liver.
This makes LDL particles more susceptible to oxidative damage
This can lead to the formation of atherosclerotic plaques

81
Q

What does ApoB100 do?

A

Binds to LDL receptors on the plasma membrane of cells of peripheral tissues requiring cholesterol
Triggers receptor-mediated endocytosis

82
Q

What does apoC do?

A

Binds to lipoprotein lipase on adipocytes and muscle

Hydrolyses TAGs
Fatty acids enter cell, (for storage in adipocytes and energy in muscle)

83
Q

What does apoE do?

A

Binds to LDL receptor on hepatocytes so chylomicron remnant is taken up by receptor mediated endocytosis. Lysosomes release remaining contents for metabolism.

84
Q

What is the primary function of HDL?

A

HDL particles remove cholesterol from cells with export cholesterol and return this cholesterol to liver for disposal as bile salts and to cells requiring additional cholesterol

85
Q

Where are HDL particles produced?

A

New HDL particles with a low TAG content are synthesised by the liver and intestine (some HDL particles can bud off from chylomicrons and VLDL as they are digested by lipoprotein lipase

86
Q

Describe the structure of HDL.

A

They have a hollow core which progressively fills as the particle accumulates phospholipid and cholesterol from cells living blood vessels.

87
Q

Why are HDL particles important?

A

They reduce the likelihood of foam cell and atherosclerotic plaque formation.

88
Q

What does free apoA-I do?

A

Free apoA-I can also acquire cholesterol and phospholipid from other lipoproteins and cell membranes to form nascent-like HDL

89
Q

How do HDL particles remove cholesterol from cells with excess cholesterol?

A
  • The ABCA1 protein within cells facilitates the transfer of cholesterol to HDL by a process known as reverse cholesterol transport
  • Cholesterol is then converted to cholesterol ester by LCAT and the mature HDL is taken up by the liver via specific receptors.
90
Q

What is the cholesterol exchange transfer protein (CETP) used for?

A

HDL can exchange cholesterol ester for TAG with VLDL particles via the action of this

91
Q

Which cells have a scavenger receptor (SR-B1) and what for?

A

Cells requiring additional cholesterol eg. For steroid hormone synthesis
They use this receptor to obtain cholesterol from HDL

92
Q

How is cholesterol disposed?

A
  • The liver disposes cholesterol by converting it to bile salts that are secreted in the bile
  • Additionally, a small amount of cholesterol is secreted directly in the bile
  • Bile salt sequestrants eg. Cholestyramine lower plasma cholesterol by increasing its disposal from the body by binding to the bile salts and preventing them from being reabsorbed into the hepatic portal circulation promoting their loss in the faeces.
93
Q

What are hyperlipoproteinaemias?

A

Raised plasma level of one or more classes of lipoprotein

Caused by either:
Under production
Under removal

Defects in:
Receptor
Apoprotein
Enzyme

94
Q

What causes familial hypercholesterolaemia?

A

Absence or deficiency of functional LDL receptors

95
Q

What are the clinical signs of hypercholesterolaemia?

A

Xanthelasma - yellow patches on eyelids

Tendon xanthoma - nodules on tendon

Corneal arcus - obvious white circle around eye. Common in older people but if present in young, could be a sign of hypercholesterolaemia

96
Q

How are hyperlipoproteinaemias treated?

A

First approach…

Diet
-reduce cholesterol, increase fibre

Lifestyle
Increase exercise
Stop smoking to reduce CVS risk

Statins

  • reduce synthesis of cholesterol in the liver by inhibiting the enzyme HMG-coA reductase
  • increased expression of lipoprotein lipase

Bile salt sequestrants
Bind bile salts in GI tract. Forces liver to produce more bile acids using more cholesterol

97
Q

Why is high serum LDL associated with atherosclerosis?

A

LDL has a long half life so is prone to oxidation

Oxidised LDL is recognised and engulfed by macrophages

Lipid laden macrophages called foam cells accumulate in the intima of blood vessel walls to form a fatty streak

Fatty streaks can evolve to form atherosclerotic plaques

This grows and can block the lumen of the artery (if in coronary arteries can cause angina)

The plaque can rupture

This triggers acute thrombosis by activating platelets and clotting cascade (stroke if in carotid arteries and myocardial infarction if in coronary arteries)

98
Q

How do statins reduce plasma cholesterol?

A

They inhibit HMG-CoA reductase which catalyses the first step of cholesterol synthesis.

However, it has side effects as it has blocked the formation of many intermediates

99
Q

Which class of lipoprotein particle typically contains the greatest amount of cholesterol and cholesterol ester?

A

LDL
The main function of LDL particles is the transport of cholesterol synthesised in the liver to tissues. You would therefore expect these lipoprotein particles to have a high total cholesterol content. ~58% of their content is cholesterol and cholesterol esters.

100
Q

Which enzyme located on the capillary walls of muscle and adipose tissue facilitates the release of fatty acids from chylomicrons and VLDL’s?

A

Lipoprotein lipase located on capillary walls hydrolyses the triacylglycerols contained in lipoprotein particles allowing uptake of fatty acids into the tissue.

101
Q

By what mechanism are LDL lipoprotein particles taken up by peripheral tissues?

A

Receptor mediated endocytosis

102
Q

Which lipoprotein particle facilitates reverse cholesterol transport?

A

HDL
HDL lipoprotein particles remove cholesterol from cholesterol-laden cells and return it to the liver. The ABCA1 protein within the cell facilitates the transfer of cholesterol to HDL. Cholesterol is then converted to cholesterol ester by LCAT

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