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Fundamentals Of The Living Cell > Lipid synthesis and degradation > Flashcards

Lipid synthesis and degradation Flashcards

1
Q

How is fat obtained?

A

Obtained either from diet or made de novo from carbohydrates

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2
Q

What role does fat play in biological functions?

A

○ Membranes
○ Uptake of lipid soluble vitamins
As precursors of steroid hormones

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3
Q

What is the relation between one gram of fat and either carbohydrate or protein?

A

Energy from one gram of fat = over twice that of either carbohydrate or protein

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4
Q

How much energy from 1 g of fat?

A

37KJ

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5
Q

How much energy from 1 g of protein?

A

17KJ

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6
Q

How much energy from 1 g of carbohydrate?

A

16KJ

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7
Q

What happens when calorific intake exceeds consumption?

A

When calorific intake exceeds consumption excess is laid down as fat

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8
Q

Where are fatty acids usually synthesised and stored?

A

Usually synthesised in liver however stored in adipose tissue

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9
Q

What do cardiac muscle use as their preferred energy source?

A

Cardiac muscle use fat as preferred energy source

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10
Q

What is the most common source of metabolic building blocks?

A

○ Dietary carbohydrate is the most common source of metabolic building blocks although some amino acids can also be used

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11
Q

What is the major product in fatty acid synthesis?

A

Palmitic acid is the major product that is modified by enzymes to produce different fatty acids

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12
Q

What is the structure of a fatty acid?

A

Chains of methyl groups with terminal carboxyl group

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13
Q

Do fatty acids have double bonds?

A

Can have double bonds and if present, usually in cis conformation

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14
Q

What are humans unable to create regarding double bonds?

A

Humans unable to create double bonds less than position 9

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15
Q

Where are essential fatty acids obtained from?

A

• Essential fatty acids obtained from diet

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16
Q

Where does fatty acid synthesis from glucose occur?

A

Occurs in cytosol

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17
Q

What happens to some citrate in fatty acid synthesis?

A

• Some citrate exported out the mitochondria and converted into acetyl CoA
○ Acetyl CoA cannot cross membrane whereas citrate can

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18
Q

What is acetyl CoA converted into and what happens to it?

A 
• Acetyl CoA converted to fatty acids:
	○ Some stay in liver
	○ Majority imported as free 
           fatty acids and 
           consumed in non-hepatic 
           tissue
           Majority stored in 
           adipocytes(have ability to 
           synthesise fats)
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19
Q

How is acetyl CoA transferred into the cytosol?

A
  • Pyruvate enters mitochondria and converted to oxaloacetate
  • Oxaloacetate combines with Acetyl CoA to form citrate
  • Citrate transported out and cleaved to form acetyl CoA and oxaloacetate
  • Oxaloacetate is converted to malate and then pyruvate

Acetyl CoA and NADPH formed

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20
Q

What activates the first step in citrate malate antiport?

A

Activated by citrate

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21
Q

What is the citrate-malate antiport inhibited by?

A

Inhibited by palmitic acid

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22
Q

What vitamin is required for the citrate-malate antiport first step?

A

Vitamin Biotin

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23
Q

What type of step is the first step in citrate-malate antiport?

A

Irreversible regulatory step

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24
Q

What is acetyl CoA carboxylase inhibited by?

A

Inhibited by phosphorylation

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25
Q

When is the expression of acetyl CoA carboxylase increased?

A

Expression of Acetyl CoA carboxylase increased by high carbohydrate and low fat

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26
Q

When is the expression of acetyl CoA carboxylase decreased?

A

Expression of Acetyl CoA carboxylase decreased by low carbohydrate and high fat

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27
Q

Where does the second step of the citrate-malate antiport occur?

A

Occurs in the cytosol

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28
Q

What does elongation mean in terms of the second step in the citrate-malate antiport?

A

Means the addition of 2C

29
Q

What occurs in the second step of the citrate-malate antiport?

A

a. Malonyl CoA formed by acetyl CoA carboxylase
i. Malonyl residue transferred to ACP
b. A second acetyl molecule from Acetyl CoA is then transferred to ACP where two condense to form Acetoacytyl-ACP
c. Fatty acid synthase is a multi-enzyme complex required for fatty acid synthesis
Exists as a dimer to make synthesis efficient as possible

30
Q

What is the structure of cholesterol?

A

Rigid hydrophobic molecule

Virtually insoluble

31
Q

What is cholesterol a precursor of?

A

Precursor of steroids, sterols and bile salts

32
Q

As what is cholesterol transported as?

A

Transported in the circulation as cholesteryl esters

33
Q

Why is cholesterol unable to provide energy?

A

Cannot be oxidised to O2 and H20 so provide no energy

34
Q

Why is cholesterol an important membrane component?

A

Important membrane component for fluidity

35
Q

Where is cholesterol mostly synthesised?

A

Mostly synthesised in the ER

36
Q

What does cholesterol synthesis start with?

A

Starts with activation of acetate, acetyl CoA

37
Q

What is the major regulatory step?

A

Major regulatory step is the conversion of 3-hydroxyl-3-methylglutaryl CoA to mevalonate

38
Q

What does cholesterol inhibit and what is that involved in?

A

• Cholesterol inhibits HMGCoA reductase

Enzyme involved in its own synthesis

39
Q

Why is it difficult to reduce circulating cholesterol by diet alone?

A

Difficult to reduce circulating cholesterol by diet alone as endogenous synthesis is increased

40
Q

In the first step of fatty acid degradation(Mobilisation adipocyte), what does cAMP activate and what is the activated molecule involved in?

A

cAMP activates protein kinase A which is involved in the breakdown of glycogen and inhibition of glycogen synthesis

41
Q

What does the activated protein kinase A do in mobilisation adipocyte?

A

Activated protein kinase A will phosphorylate and activate triacylglycerol lipase, removing fatty acid from glycerol

42
Q

What breaks down triaglycerol and what is formed?

A

Phosphorylated triacylglycerol lipase breaks down triacylglycerol to form diacylglycerol and transported via lipoproteins or bound to albumin.

43
Q

What component goes back to the liver?

A

One of the components, glycerol, get back to the liver as its the only part of the fatty acid which can be used to make glucose

44
Q

Where are fatty acids transported and what are they activated by?

A

Fatty acids transported to liver and activated by acyl-CoA synthase in the cytoplasm

45
Q

What happens to the acetyl CoA which is produced?

A

Acetyl CoA produced is transported across the inner mitochondrial membrane bound to the alcohol carnitine

46
Q

In the second step of fatty acid degradation(activation), where does it occur?

A

Occurs in the liver cytosol

47
Q

How are the fatty acids activated?

A

FA activated by reacting with CoA requiring ATP

48
Q

Where are the fatty acids transported using what and for what purpose?

A

Transported to inner mitochondrial matrix for oxidation using carnitine

49
Q

What inhibits the transport of fatty acids?

A

Transport inhibited by malonyl-CoA

50
Q

What does it mean therefore if there is a large amount of malonyl CoA?

A

i. So large amounts of malonyl CoA prevents breakdown when excess glucose is present

51
Q

In the third step of fatty acid degradation(degradation), what is Acyl-CoA degraded by

A

Degraded by sequential removal of 2C units

52
Q

As a result of the degradation of acyl-CoA, what is produced?

A

FADH2, NADH and acetyl-CoA

53
Q

What are used for glycolysis from the products formed from the degradation of acyl-CoA?

A

FADH2 and NADH

54
Q

What forms ATP in fatty acid oxidation(Beta-oxidation)?

A

FADH2 and NADH

55
Q

When does acetyl CoA only enter the citric acid cycle?

A

Only in the presence of glycolysis

56
Q

How many ATP molecules do we get from the complete oxidation of palmitic acid?

A

106 molecules of ATP

57
Q

What type of chain yield is in last round of oxidation?

A

Odd chain length yield propionyl-CoA in the last round of oxidation

58
Q

How are odd numbered double bonds removed?

A

Removed by isomerase

59
Q

How are even numbered bonds removed?

A

Even numbered bonds removed by reductase and isomerase

60
Q

What is acetyl CoA in hepatocytes converted into and transported where?

A

Acetly-CoA in hepatocytes converted to ketone bodies and are transported to non hepatic tissue for metabolism

61
Q

In ketogenisis, what is acetyl CoA converted into?

A

Acetyl-CoA converted to acetoacetyl-CoA

62
Q

What is acetoacetyl -CoA converted into?

A

Converted to HMG-CoA

63
Q

What is HMG-CoA converted into?

A

Converted to acetoacetate

64
Q

What can acetoacetate be reduced to?

A

Acetoacetate can be reduced to 3-β-hydroxybuterate or non-enzymatically to acetone

65
Q

When is the rate of ketogenisis high and why?

A

Ketogenisis high when ration of insulin/glucagon is low as this inhibits acetly-CoA carboxylase

66
Q

What are ketones a major energy source for?

A

Major energy source for cardiac muscle and renal cortex

67
Q

How does insulin regulate fat metabolism?

A

○ Increases glycolysis in the liver
○ Increases fatty acid synthesis in the liver
○ Increases triglyceride in adipose tissue

Decreases β-oxidation

68
Q

How does glucagon regulate fat metabolism?

A

Glucagon increases triglyceride mobilisation

69
Q

What happens during starvation?

A

During starvation up to 75% of the brains energy is derived from acetoacetate.

Fundamentals Of The Living Cell (31 decks)

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