Lipids Flashcards

(42 cards)

1
Q

Are lipids structurally diverse? are they soluble? what do they contain (element-wise)? Are they more or less reduced than carbohydrates? what does this do to energy released and O2 need?

A

Lipids are structurally diverse, insoluble in water (hydrophobic), mostly only contain C, H, O, more reduced than carbohydrates = more energy released when oxidised, complete oxidation requires more O2

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2
Q

What are the 3 classes of lipids?

A

Fatty acid derivatives, Hydroxy-methyl-glutaric acid derivatives, Vitamins

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3
Q

What are the 4 derivatives of fatty acids and what are their roles?

A

Fatty Acids – Fuel molecules
Triacylglycerols – Fuel storage and insulation
Phospholipids – Components of membranes and plasma lipoproteins
Eicosanoids – Local mediators

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4
Q

What are the 4 derivatives of hydroxy-methyl-glutamic acid and what are their roles?

A

Ketone bodies (C4) – Water soluble fuel molecules
Cholesterol (C27) – Membranes and steroid hormone synthesis
Cholesterol esters – Cholesterol storage
Bile acids and salts (C24) – Lipid Digestion

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5
Q

What are there 4 fat-soluble vitamins?

A

A, D, E and K

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6
Q

What is the general structure of a triaglycerols (TAG)?

nb. triaglycerols = triglycerides

A

Glycerol backbone, 3 fatty acid side chains. connected by ester bonds

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7
Q

What is chemical formula for glycerol and general formula for fatty acids?

A

glycerol = C3H8O3

Fatty acid = CH3(CH2)nCOOH

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8
Q

What is process for forming/breaking down triaglycerol?

A

forming = esterification, breaking down = lipolysis

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9
Q

Where are triaglycerols stored and in what form? what is their role? how are they controlled?

A

Stored in adipose tissue, in anhydrous form, used in prolonged exercise, starvation and pregnancy. storage/utilisation is under hormonal control

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10
Q

How and where are triaglycerols broken down. what else is needed (apart from the enzymes)?

A

pancreatic lipase in the small intestine to release glycerol and fatty acids. This is a complex process requiring bile salts and a protein factor called colipase

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11
Q

What happens in the small intestine to the glycerol and fatty acids?

A

recombined and transported as TAG by lipoproteins (chylomicrons)

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12
Q

Where do the lipoproteins carry the TAG to and what happens to the TAG?

A

Consumer tissues - fatty acid oxidation -> energy

Adipose tissue - stored as TAG

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13
Q

How does TAG in the adipose tissue get used by consumer tissues?

A

There is hormone-sensitive lipase which becomes more active in the presence of adrenaline/glucagon (less active in presence of insulin). Fatty acids transported by albumin, where it is oxidised to give energy

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14
Q

What is the general formula for Fatty acids?

A

CH3(CH2)nCOOH where n = 14 - 18

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15
Q

What is the difference between a saturated and a non-saturated fatty acid?

A

unsaturated has 1 or more double bonds C=C, saturated has none

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16
Q

what is an amphipathic fatty acid?

A

contains hydrophilic and hydrophobic groups

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17
Q

why are certain polyunsaturated fatty acids essential?

A

mammals can’t introduce a double bond beyond C9

18
Q

Where does fatty acid catabolism take place?

A

in mitochondria

19
Q

What happens in FA catabolism (in brief)

A

FA is activated by linking to coenzyme A outside mitochondrion, then transported across inner mitochondrial membrane using a carnitine shuttle, then cycles through sequence of oxidative reactions, with C2 removed every cycle

20
Q

How is FA activated? give equation

A

links to coenzyme A by action of fatty acyl coA synthase CH3(CH2)nCOOH + ATP + CoA -> CH3(CH2)nCO-CoA + AMP + 2Pi

21
Q

Can activated fatty acids cross mitochondrial membrane?

22
Q

How does carnitine shuttle work?

A

Acyl-CoA binds to carnitine with Carnitine acyltransferase (CAT I), forming Acyl carnitine and CoA (so CoA is reused)
Acyl Carnitine crosses inner mitochondrial membrane via the carnitine shuttle transporter ( carnitine-acylcarnitine translocase)
Acylcarnitine + CoA is converted to acyl-CoA by carnitine acyltransferase II (CAT II) and carnitine is released into cytosol and passes back into inter membrane space to bind with another Acyl-CoA

23
Q

Is the carnitine shuttle regulated?

A

yes - so controls rate of FA oxidation

24
Q

What is the carnitine shuttle inhibited by?

25
What are the reactants and products of fatty acid catabolism (β-oxidation)?
reactants: fatty acid, FAD, H2O, NAD+, CoA, ATP products: acetyl-CoA, AMP, Pi, FADH2, NADH, H+
26
Which products from the catabolism of FA are used to make ATP?
Acetyl-CoA - used in TCA cycle | FADH2, NADH + H+ - used in oxidative phosphorylation
27
Which oxidation produces more ATP - glucose or FA?
FA
28
Where is glycerol metabolised?
liver
29
How is glycerol converted to glycerol phosphate? (enzyme and reactants)
Glycerol + ATP -> Glycerol Phosphate + ADP (enzyme = glycerol kinase)
30
What are the 2 possible outcomes for the glycerol phosphate?
Triaglycerol synthesis Enter glycolysis after being dehydrogenated by NAD+ and Glycerol-3-phosphate dehydrogenase to form Dihydroxyacetone phosphate (DHAP) (which enters glycolytic pathway)
31
What are the 3 ketones produced in the body?
Acetoacetate, acetone and β-hydroxybutyrate
32
What is normal plasma ketone body conc? Range of conc during starvation? Conc in untreated type 1 diabetes?
10mM (pathological ketosis)
33
Where are Acetoacetate and β-hydroxybutyrate formed and by what? How is acetone formed?
Formed in liver by mitochondria using acetyl-coA. acetone is formed by the spontaneous non-enzymatic decarboxylation acetoacetate and β-hydroxybutyrate
34
Are ketones soluble? If so, what does this allow?
Ketone bodies are water-soluble molecules, allowing high plasma concentration and excretion in urine (ketonuria)
35
How does acetone cause the "sweet smell" in breath of type 1 diabetics?
Acetone is produced. Acetone is volatile and may be excreted via the lungs
36
How can an accumulation of acetoacetate and β-hydroxybutyrate cause ketoacidosis?
Acetoacetate and β-hydroxybutyrate are relatively strong organic acids and when in high concentration in the plasma they may cause acidosis.
37
When does ketone synthesis occur?
When glucose concentration is low. (eg. starvation/diabetes) Therefore ↓Glucose ↑Glucagon ↑Hydroxymethyl glutaryl CoA Lyase (enzyme used in synthesis of ketones from Hydroxymethyl glutaryl-CoA ↑Ketones Works as Lyase inhibits reductase so less mevalonate formed and more ketones formed
38
Which enzyme is involved in ketone regulation? What does this do?
Hydroxymethyl glutaryl CoA reductase. converts Hydroxymethyl glutaryl-CoA into mevalonate which forms cholesterol
39
What does the synthesis of ketone bodies require?
Fatty acids to be available for oxidation in the liver following excessive lipolysis in adipose tissue – this supplies the substrate. The plasma insulin/glucagon ratio to be low, usually due to a fall in plasma insulin – this activates the lyase and inhibits the reductase
40
How can ketone bodies be used to produce ATP?
Increase in conc causes ketones to be converted to acetyl-CoA which is oxidised via stage 3 catabolism (TCA cycle)
41
What is acetyl-coA produced by the catabolism of?
Fatty Acids, sugars, alcohol, certain amino acids
42
How can acetyl-coA be used to produce ATP?
Can be oxidised via stage 3 of catabolism (TCA cycle)