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MEH > Session 2 - energy storage > Flashcards

Session 2 - energy storage Flashcards

1
Q

Three energy stores in the human body?

Which contains the most and least energy?

A
  • Triacyclglycerols (fat)
  • Muscle protein
  • Glycogen

Most - triacylglycerols
Least- glycogen

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2
Q

A fasting period of ___ hours depletes glycogen stores?

How will you maintain blood glucose?

A

8-10 hours

gluconeogenesis

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3
Q

Why is glycogen highly branched?

Which bonds does it contain?

A

So there’s lots of sites to add or remove glucose residues quickly

glycosidic bonds;

  • alpha 1-4
  • alpha 1-6
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4
Q

Where is glycogen stored and in what form?

How much glycogen is stored here in grams?

A

Granules in the liver and skeletal muscle

liver > 100g
skeletal muscle > 300g

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5
Q

What limits how much glycogen can be stored?

A
  • Highly polar molcule which attracts a lot of water into the tissue
  • The tissues are not specialised for storage and must perform other functions
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6
Q

What is the advantage of glycogen’s large size?

A

Lots of glucose molecules can be stored with minimal osmotic effect

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7
Q

How is glucose added to the glycogen molecule?

A
  • First converted to glucose-6-phosphate by adding ATP (hexokinase)
  • Converted to glucose-1-phosphate by moving the phosphate group (phosphoglucomutase)
  • UTP added to make highly activated UDP- glucose
  • UDP glucose added to glycogen
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8
Q

Which enzyme(s) add the final glucose intermediate to glycogen?

Is this reaction reversible?

A

UDP- glucose

  • glycogen synthase adds residues in series (alpha 1-4 bond)
  • branching enzyme adds a glucose via alpha 1-6 bond every 10 units

NO it is irreversible; a separate and distinct mechanism exists for glycogen degradation

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9
Q

Which enzyme converts free glucose to glucose-6-phosphate?

  • In the liver
  • In skeletal muscle
A

glucokinase (liver)

hexokinase (muscle)

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10
Q

When is glycogen broken down from its stores?

A

Muscle- during exercise

Liver- fasting or fight/flight response

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11
Q

Name the sugar intermediates in glycogen degradation

A

Glycogen (n residues)
Glucose-1-phosphate
Glucose-6-phosphate
Glucose

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12
Q

Why is glucose released from glycogen as glucose-1-phosphate?

Which enzyme breaks the alpha 1-6 bonds?

A

The alpha 1-4 bonds are subjected to phosphorolysis by glycogen phosphorylase

de-branching enzyme

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13
Q

When is free glucose released from glycogen?

A

When the alpha 1-6 bond is hydrolysed by de-branching enzyme

(instead of phosphorolysis by the alpha 1-4 bond by glycogen phosphorylase)

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14
Q

Where does the glucose released from glycogen stores end up?

Why is the destination different?

A

Muscle- glucose-6-phosphate enters glycolysis to supply muscle with energy (ATP)

Liver- free glucose enters the bloodstream to supply other tissues

The liver can break down glucose-6-phosphate into free glucose which the muscle cannot.
(Liver has glucose-6-phosphatase)

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15
Q

Which enzyme catalyses this reversible reaction?

glucose-1-phosphate <> and glucose-6-phosphate?

A

phosphoglucomutase

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16
Q

Which enzyme facilitates liver glycogen to be an energy store for the whole body?

A

glucose-6-phosphatase

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17
Q

Which two hormones upregulate glycogen breakdown?

Which one hormone promotes glycogen synthesis?

How do the hormones have this effect?

A
  • Glucagon
  • Adrenaline
    Increase the activity of glycogen phosphorlyase
    (thus reducing that of glycogen synthase)
  • Insulin
    Increases activity of glycogen synthase
    (thus reducing that of glycogen phosphorylase)
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18
Q

What is covalent modification?

What mechanism activates;

  • glycogen phosphorylase
  • glycogen synthase
A

Phosphorylation / de-phosphorylation

  • phosphorylation
  • de-phosphorylation
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19
Q

AMP allosterically modifies which enzyme involved in glycogen metabolism?

Where can it have this action?

A

AMP (low energy molecule) binds glycogen phosphorylase to increase glucose release

Skeletal muscle glycogen ONLY

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20
Q

Where does gluconeogenesis occur?

What’s the exception?

A

liver

in starvation, the kidney cortex can produce glucose

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21
Q

What is used to make glucose in gluconeogenesis?

A

amino acids

glycerol/ pyruvate/ lactate

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22
Q

Why can’t acetyl CoA be used to make glucose in gluconeogenesis?

A

Bc the reaction which converts pyruvate to Acetyl CoA is irreversible
(catalysed by pyruvate dehydrogenase, PDH)

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23
Q

Which 4 enzymes are important in converting pyruvate to glucose?

A

(The enzymes bypass the 3 irreversible reactions (1, 3, 10) of glycolysis to reverse pyruvate)

  • Pyruvate carboxylase
  • PEPCK
  • Fructose 1,6- bisphosphatase
  • glucose-6-phosphatase
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24
Q

What do Pyruvate carboxylase and PEPCK do?

A

Pyruvate carboxylase converts pyruvate to oxaloacetate (OAA)

PEPCK converts oxaloacetate to PEP (phosphoenolpyruvate) which can enter reverse-glycolysis

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25
Q

What does fructose-1-6- bisphosphatase do?

A

Bypasses step 3 of (reverse) glycolysis to generate glucose from pyruvate

Converts fructose- 1,6- bisphosphate to glucose-6-phosphate

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26
Q

Which enzyme converts glucose-6-phosphate back to free glucose?

Which glycogen storage organ has this enzyme?

A

glucose -6- phosphatase

liver NOT skeletal muscle

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27
Q

Oxaloacetate is converted to PEP in gluconeogenesis.

Where is oxaloacetate made?

A
  • From pyruvate by pyruvate decarboxylase
  • Transamination of aspartate in amino acid metabolism
  • Intermediate in TCA/ citric acid cycle (C4)
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28
Q

How do hormones regulate gluconeogenesis?

How does this relate to diabetes?

A
  • Glucagon and cortisol increase the activity of PEPCK and fructose-1,6- bisphosphatase
  • Insulin reduces their activity

In diabetes, insulin is deficient. Thus glugoneogenesis can’t be downregulated and can contribute to the characteristic fasting hyperglycaemia

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29
Q

Lipid storage is under ____ control?

How?

A

Hormonal control

Hormones affect the activity of Acetyl CoA carboxylase (key regulatory enzyme of lipid storage)

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30
Q

Which is the key regulatory enzyme of lipid storage?

What does the enzyme do?
Which co-factor does it require?

A

Acetyl CoA carboxylase

  • Converts Acetyl CoA to Malonyl CoA (C3) which can then be added to the fatty acid chain
  • Added by fatty acid synthase complex
  • Thus it regulates synthesis of fatty acids; which are converted to TAG for storage

Biotin

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31
Q

How do fatty acids chains grow?

A 
Malonyl CoA (C3) is added at the expense of CO2 
(2 carbons added at a time)
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32
Q

Which hormones upregulate Acetyl CoA carboxylase?

Which hormones down regulate activity?

How do the hormones have these effects?

A

(Upregulate; increase lipid storage)
Insulin

Downregulate; reduce lipid storage

  • Glucagon
  • Adrenaline
  • Growth hormone
  • Cortisol
  • Thyroxine

Promote dephosphorylation to activate
Promote phosphorylation to inhibit

33
Q

Phosphorylation/ dephosphorylation
Which activates Acetyl CoA carboxylase?
What effect does this have on lipid storage?

A

Dephosphorylation activates Acetyl CoA which increases lipid storage

34
Q

Why are triacylglycerols an efficient method of storing energy?

How are fatty acids converted to TAG’s?

From what are fatty acids synthesised?
How is this molecule obtained?

A

Can be stored in bulk in an anhydrous form in adipose tissue

Esterification

Acetyl CoA
Citrate from the TCA cycle is cleaved in the cytoplasm to release Acetyl CoA and oxaloacetate (OAA)

35
Q

How is Acetyl CoA regulated by allosteric modification?

A

AMP (low energy molecule) binding reduces lipid storage (inhibits the enzyme)

Citrate (high energy molecule) binding activates the enzyme; promoting lipid storage

36
Q

What are the advantages of having two separate pathways for catabolism and anabolism?

A
  • More flexible (different substrates and intermediates)
  • Better control (controlled together or independently)
  • Bypass thermodynamically irreversible steps
37
Q

How are fatty acids broken down?

What is produced?

A

Cycles of Beta oxidation which remove 2 carbons each time

  • Acetyl CoA because the 2 carbons are removed as this
  • NADPH & FAD2H (oxidising agents)
38
Q

Fatty acid oxidation vs synthesis

  • Where do they occur?
  • Where are the enzymes located?
  • Regulated directly or indirectly?
A

Fatty acid oxidation;

  • mitochondria
  • enzymes in the mitochondrial matrix
  • regulated indirectly by the availability of fatty acids in the mitochondria

Fatty acid synthesis;

  • cytoplasm
  • multi enzyme complex in the cytoplasm (fatty acid synthase)
  • regulated directly by activity of Acetyl CoA carboxylase
39
Q

Is fatty acid synthesis an oxidative or reductive process?

A

Reductive

oxidises NADPH > NADP

40
Q

4000- 8500mg/L

What does this refer to?

A

Total lipids in the blood

41
Q

Why do the levels of fatty acids in blood not normally exceed 3mmol/L?

A

They circulate bound to albumin which has a limited capacity to transport fatty acids

42
Q

In lipoproteins, how do the lipids and proteins bind?

What determines the function of a lipoprotein?

A

non-covalent interactions (mostly hydrophobic)

The composition of apoproteins

43
Q

What are the structural and functional roles of apoproteins?

A

Structural- package lipids into a soluble form due to amphipathic properties
Functional - activate enzymes, cell recognition (surface receptors)

44
Q

What does LCAT enzyme do?

When does a lipoprotein become unstable?

A

(Lecithin cholesterol acyltransferase)

Converts surface lipid to core lipid to maintain stability of the lipoprotein particle.
Cholesterol to cholesterol ester using phosphatidylcholine (fatty acid derived from lecithin)

Unstable when spherical shape is not maintained bc core lipid has been removed (the ratio of core to surface lipid has changed)

45
Q

What does the core and coating of a lipoprotein contain?

A

Core; cholesterol esters, triacylglycerols

Coating; cholesterol (amphipathic), apoproteins, phospholipids

46
Q

5 classes of lipoproteins?

How can they be separated?

A 
chylomicrons
VLDL
IDL
LDL
HDL

Ultracentrifugation/ electrophoresis due to different protein and lipid compositions

47
Q

What do VLDL’s do?

Where do LDL’s come from and what do they do?

A

Transport TAG’s synthesised in the liver to adipose tissue for storage

Removal of lipid from VLDL leads to IDL (intermediary) and LDL’s
LDL’s transport cholesterol made in the liver to tissues

48
Q

Why are HDL’s considered the good cholesterol?

A

Transport excess tissue cholesterol to the liver for disposal as bile salts / to cells requiring cholesterol

49
Q

What are chylomicrons?

A

Dietary lipids being carried in the blood

50
Q

How are dietary lipids used as fuel?

A
  • They can’t be absorbed directly so are hydrolysed by pancreatic lipases to fatty acids (FA) and glycerol
  • FA’s enter the epithelial cells and are re-esterified back to TAG which are packaged into chylomicrons
  • chylomicrons are released from epithelial cells into the lymphatics system
  • Enter the blood at the thoracic duct (lymph duct in the thorax) which empties into the left subclavian vein
  • Chylomicrons carried to tissues (e.g. adipose)
  • lipoprotein lipase in the tissue’s capillaries hydrolyses the core TAG’s to release fatty acids which enter the cell
  • in muscle tissue they’re used for energy production
51
Q

In what form can lipid enter a cell?

Where do you find lipoprotein lipase?
How is it regulated?

A

As a fatty acid

Inner surface of capillaries (endothelium)
Insulin increases synthesis of the enzyme

52
Q

Which apoprotein is added to VLDL’s during formation?
Which 2 are added after and where do they come from?
Where are VLDL’s made?

A

apoB100
apo C and E from HDL in the blood

Made in the liver

53
Q

When does a VLDL become a LDL?
How does this occur?

Is an LDL high/ low cholesterol?

A

When the core TAG depletes to 10% of initial content and apo C and apo E have dissociated
(30% is IDL)

TAG is removed by lipoprotein lipase which hydrolyses the molecules to fatty acids and glycerol.

High cholesterol particle

54
Q

How do cells obtain the cholesterol from LDL’s?
What is the cholesterol used for?

How does this process stop cells accumulating too much cholesterol?

A

Receptor mediated endocytosis of the LDL- LDL receptor complex followed by lysosomal digestion which converts cholesterol esters to free cholesterol released into the cell

  • Stored by the cell as cholesterol esters
  • Used by the cell

Inhibits cholesterol synthesis by the cell and reduces the synthesis and expression of LDL receptors on the cell surface

55
Q

How do cells recognise LDL’s?

A

Cell surface LDL receptors which bind ApoB100

56
Q

LDL’s are linked to the formation of ____ ___?

How does this occur?

A

atherosclerotic plaques
(athero- in arteries)

  • LDL is oxidised by ROS
  • Recognised and engulfed by macrophages.
  • Foam cells accumulate in the intima of blood vessel walls to form a fatty streak
  • Fatty streak evolves into atherosclerotic plaque
57
Q

Why are LDL’s linked to atherosclerosis rather than VLDL’s?

A

They have a longer half life in blood bc they’re not efficiently cleared by the liver so are more susceptible to oxidative damage

58
Q

What’s a foam cell?

A

Lipid laden macrophages

engulfed lots of oxidised LDL

59
Q

What conditions can an atherosclerotic plaque cause?

A
  • Angina if the plaque encroaches on the lumen
  • MI/ Stroke if it ruptures and triggers acute thrombosis
    (by activating platelets and the clotting cascade)
60
Q

What is familial hypercholesterolaemia?

What condition does it predispose to?

A

Absence/ reduced expression of LDL receptors leading to an accumulation of LDL’s and cholesterol in the blood which predisposes to atherosclerosis

Absence = homozygous mutation
Reduced expression = heterozygous

61
Q

Cells in need of cholesterol express which receptor?

Which cells could this be?

A

Scavenger receptor SR-B1
to bind HDL’s

Those involved in steroid hormone synthesis

62
Q

What does cholesterol exchange transfer protein do?

A

Facilitates exchange of cholesterol esters from HDL’s for TAG from VDL’s

63
Q

Where are HDL’s synthesised?
Is the initial TAG content high or low?

HDL’s take cholesterol from cells by what process?

A

Liver and intestine
Low initially, they accumulate lipid as they remove phospholipid and excess cholesterol from cells

reverse cholesterol transport
free excess cholesterol is converted to cholesterol ester by LCAT for transport in the HDL

64
Q

Which protein facilitates transfer of cholesterol to HDL’s?

A

ABCA1 protein

65
Q

Dyslipoproteinaemias

what are they?

A

Any error in the metabolism of plasma lipoproteins

66
Q

How do you classify the hyperlipoproteinaemias?
How many types are there?

They all increase the risk of which condition?

A

Fredrick system
6
(2a &2b)

Coronary artery disease
- reduced blood flow to the heart due to plaques in the vessels)
(excess cholesterol in plasma increases risk of atheroscleroma)

67
Q

What’s another name for coronary heart disease?

A

Ischaemic heart disease

68
Q

Type 1 , 2a, 3
hyperlipoproteinemias
- what is it categorised by?
- What is it caused by?

A

Type 1

  • High chylomicrons in plasma
  • No lipoprotein lipase receptor

Type 2a

  • No LDL receptor
  • High LDL’s in plasma

Type 3

  • No apoE
  • High IDL’s and chylomicron remnants
69
Q

What are chylomicron remnants?

A

What’s left after TAG have been removed from the core chylomicron

70
Q

Which 2 drugs may be given in hyperlipoproteinaemias?
Give an example

How do they work?

A
  • Statins (atvorstatin)
  • Bile salt sequestrants (cholestyramine)

Statins

  • inhibit synthesis of cholesterol in the liver by inhibition of HMG CoA reductase
  • upregulate expression of lipoprotein lipase

bile salt sequestrants
- bind bile salts in bile to prevent reabsorption; thus increasing cholesterol excretion from the body

71
Q

How can the liver excrete cholesterol?

A
  • Secrete directly into bile

- Convert to bile salts in bile

72
Q

Two pathways cells can obtain cholesterol?

A
  • receptor mediated endocytosis of LDL receptors

- synthesis inside the cell from Acetyl CoA

73
Q

3 signs/ symptoms of very high blood cholesterol?

A
  • Accelerated development of atherosclerotic diseases
  • Corneal arcus *
  • Xanthelasma** &/or tendon xanthoma”

*White arcs on the cornea due to depositis of cholesterol
** Yellow patches on inside of eyelids which fill with cholesterol
“ nodules on tendons due to cholesterol deposition

74
Q

Which hormones stimulate gluconeogenesis?

A

cortisol and glucagon

75
Q

Describe how TAG’s stored in adipose tissue can be used as fuel by skeletal muscle cells

A
  • TAG’s are hydrolysed to fatty acids and glycerol by hormone-sensitive lipase (lipolysis)
  • Fatty acids carried in blood bound to albumin (non-covalent interactions)
  • Enter target cells and are activated by linking to Acetyl CoA
  • Transported into mitochondria for beta oxidation using the carnitine shuttle
  • Cycles of beta oxidation occur until the fatty acid chain has only 2 C’s; it is Acetyl CoA
  • Acetyl CoA enters the TCA cycle to generate ATP
76
Q

What stimulates lipolysis?

A

Starvation, prolonged aerobic exercise, stress situations and lactation

  • glucagon
  • Adrenaline
  • Growth hormone
  • Cortisol
  • Thyroxine
77
Q

What is synthesised from Acetyl CoA?

Why can it not be synthesised to glucose?

A

Most lipids + ketone bodies

It can’t be converted to pyruvate (and hence glucose) bc the enzyme which converts pyruvate to acetyl CoA is irreversible and there is no other mechanism to bypass the enyzyme
(pyruvate dehydrogenase)

78
Q

Heinz bodies are a sign of what?

A

G6PDH deficiency

ROS damage in red blood cells causing inappropriate cross linking of disulphide bonds in haemoglobin

MEH (9 decks)

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