Lipid Oxidation / Metabolism Flashcards

(59 cards)

1
Q

What are fats stored as for energy source

A

Triglycerides- glycerol and 3 fatty acids

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2
Q

Where are triglycerides/ fat stores found

A

In adipose fat tissues under the skin eg in bum

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3
Q

What are the adipose tissues made from

A

Lipocytes/ adipocytes which have a nuclei and mitochondria and triglycerides

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4
Q

How is energy generated from triglycerides

A

Energy generated from the oxidation (removal of H and E) from carbon

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5
Q

Why is fat a better storage molecule than glycogen

A

Because less oxygen is present in fatty acids (only on carboxylic acid) , this means they remain reduced longer

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6
Q

What are the 3 functions/ advantages of triglycerides storage for energy in adipose tissues

A

1- FA weigh less than glucose = concentrated storage

2- end result is h20 due to hydrolysis = provides h20 storage in eg camels which store fats for water

3- insulation- under skin and electrical as myelin sheath

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7
Q

Why lipid is not used for energy storage and why

A

Cholesterol - needs combustion to break down

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8
Q

How is glycerol linked to fatty acids

A

An ester O bond (loss of water when condensation occurs)

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9
Q

Where are fatty acids condensed

A

When they are saturated due to hydrophobic interaction and no kinks

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10
Q

Explain the difference between unsaturated Cis and trans bonds

A

Trans = double bond occurs diagonally (c are further apart) = causes straight chain

CIs = carbons are on same side so close to each other— try to repel eachother causing a bend in the fatty acid

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11
Q

Why are unsaturated fats termed healthier than the saturated fatty acids

A

Easier to metabolise (not stored often)

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12
Q

What is glycerol

A

An alcohol

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13
Q

What is it called when lipids/triglycerides are broken down for energy

A

Lipolysis

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14
Q

Which enzyme activated by hormones such as epinephrine and glucagon causes lipolysis

A

Lipase enzyme - when body is in starvation mode or exercising (low BGC)

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15
Q

What does lipase do in lipolysis

A

Hydrolyses the ester bond in triglycerides forming free glycerol and fatty acids

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16
Q

Where is glycerol transported to after lipolysis by lipase

A

The liver

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17
Q

Explain the first step of how glycerol is converted to glycerol 3 phosphate

A

Glycerol kinase first uses atp hydrolysis to phosphorylate glycerol

Forming glycerol 3 phosphate

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18
Q

How is glycerol 3 phosphate then converted to dihydroxyacetone phosphate

A

Glycerol phosphate dehydrogenase which reduced NAD to form NADH and oxidised glycerol 3 phosphate

Forming dihydroxyacetone phosphate

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19
Q

How is dihydroxyacetone phosphate then converted to glyceraldehyde 3 phosphate in catabolism of glycerol (oxidation)

A

Using triose phosphate isomerase

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20
Q

What can happen with the glycerol oxidation into glyceraldehyde 3 phosphate

A

Gluconeogenesis (converted back)

or go to pyruvate for glycolysis

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21
Q

How does fatty acid oxidation differ to glycerol

A

It can’t be used for gluconeogenesis

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22
Q

What needs to happen to fatty acids before they can be oxidised

A

Activation by the addition of coA to form fatty acyl coA

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23
Q

How is fatty acid converted into fatty acyl coA in activation

A

Acyl coA synthetase catalyses the thioester bond forming between coA and fatty acid

ATP is fist hydrolysed by pyrophosphorylase which adds 2 phosphates providing energy for the formation of fatty acyl coA

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24
Q

Where does formation of acyl coA from fatty acids occur

A

In cytoplasm near the mitochondria

25
Where does oxidation of fatty acids occur
In the mitochondrial matrix
26
What is acyl coA converted to to be able to cross the mitochondrial membrane
Acyl carnitine
27
How is acyl coa converted to acyl carnitine
Loss of coA and addition of acyl to carnitine By carnitine acyl transferase 1
28
How can acyl carnitine pass the mitochondrial membrane
Because it is recognised by a membrane protein
29
How is acyl carnitine when in the matrix converted back to acyl coa and carnitine is recycled
Carnitine acyl transferase 2 | will add coA from the citric cycle to the free acyl when is is removed from carnitine
30
What is the first step of B oxidation of fatty acids (fatty acyl coA)
Fatty acid is oxidised (removal of 2 H) to reduce fad into FADH2 This creates a c=c double bond
31
What happens when fatty acid is oxidised by reduction of fad into FADH2
water is added to provide the oxygen for full b oxidation
32
What happens next to the water added in b oxidation
It is dehydrogenated by the reduction of nad to NADH2
33
Which carbon is oxidised by the oxygen in b oxidation
The beta carbon c=c turned into c = o
34
What happens when beta carbon is oxidised
Acetyl coA forms which is then released when a new coA is present to restart the b oxidation process with another carbon down the fatty acid
35
What can happen to the acetyl coA formed in b oxidation of fatty acids
Can be used in the citric cycle for glucose catabolism
36
Which source is preferred for energy, glycogen or lipids
Lipid oxidation - glycogen only used by brain or red blood cells
37
Why is acetyl coA converted into ketones
When there is low glucose in cells (diabetes or starvation) this means not enough intermediates produced from glycolysis, acetyl coA is in high supply due to lipid oxidation and builds up to produce ketones
38
What hormone suppresses fatty acid oxidation into acetyl coA which isn’t present in diabetes = build up
Insulin
39
Where does Ketogenesis occur
In the liver
40
How are 2 acetyl coA used to produce ketone bodies explain the first step
2 acetyl coa firsf have 1 coA released Forms acetoacetyl coA
41
Explain second step of ketogenesis
Acetoacetyl coA has another acetyl coA added and H2O Releases 1 coa Forming hydroxy - 3 - methyl- glutaryl coA
42
What happens to hydroxy 3 methyl glutaryl coA
Loses 1 acetyl coA forming acetoacetate
43
Which 2 ketone bodies are produced from acetoacetate
Acetone and 3 hydroxy butyrate
44
How is acetone produce from acetoacetate
H+ is added to remove a co2
45
How is 3 hydroxyl butyrate produced from aceto acetate
NADH 2 is oxidated and reduces acetoacetate into 3 hydroxy butyrate
46
What is fatty acid synthesis promoted by
Insulin (which inhibits lipolysis)
47
Is fatty acid synthesis favoured or not
No , it is endergonic
48
How does Lipo genesis differ to fatty acid synthesis
Acetyl coA is converted to fatty acids instead of fatty acids being coursed into acetyl coA for energy
49
What is needed for lipogenesis to occur
The acyl group and also addition of Malonyl coA group
50
How is acetyl coa converted to malonyl coA for lipogenesis
Acetyl coA and co2 is converted into malonyl coA By acetyl coA carboxylase (uses ATP hydrolysis for energy)
51
Which enzyme is controlled to control lipogenesis
Acetyl coA carboxylase
52
What are the positive modulators and negative modulators for acetyl coA carboxylase
+ = acetyl coA and citrate build up - = glycogen AMP Adrenaline Excess fat They indicate that glucose breakdown is needed which is helped by lipolysis
53
What happens in lipogenesis which is different to lipolysis
Acyl + malonyl Condensation Reduction Dehydration (instead of addition of h20) Reduction (instead of b oxidation) Forming acyl group + 2c = growing fatty acid
54
What is ACP and why is it needed for lipogenesis
Acyl carrier protein which is an enzyme complex which stops the loss of fatty acids in lipogenesis
55
How is it thought that excess fatty build up in the liver due to Lipogenesis can cause type 2 diabetes
B cells in the pancreas hide from the lipids and therefore causes B cell de differentiation which causes increase BGC
56
Where does synthesis of lipogenesis occur
In the matrix
57
What are the activation carrier proteins in lipogenesis vs lipolysis
Lipolysis = coA which activates fatty acids oxidation Lipogenesis = acyl carrier proteins (ACP)
58
What are the electron carriers in Lipogenesis (when they are oxidised to reduce acyl and malonyl into fatty acids) vs lipolysis (oxidation occurs via reduction of electron carrier)
Lipogenesis = NADPH which is oxidised Lipolysis = nad and fad in b oxidation which are reduced
59
Why is ketogenesis important in some cases if not in high amounts like diabetics
Because it generates atp from acetyl coA which is emergency for the brain and rbcs