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MCBHD- Molecular and Cellular Basis of Health and Disease > S2: Lipid Synthesis and Degradation > Flashcards

S2: Lipid Synthesis and Degradation Flashcards

1
Q

How are fats obtained?

A
  • In the diet

- Made de novo from carbohydrates

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2
Q

Roles of fats

A
  • Membranes
  • Important in uptake of fat soluble vitamins
  • Used as precursors for steroid hormones
  • Energy store
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3
Q

Compare energy content of fat, protein and carbohydrate

A

Fat>Protein>Carbohydrate

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4
Q

List 3 main types of fat

A
  • Fatty acids
  • Triglycerides or Neutral Fats
  • Cholesterol
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5
Q

What is the preferred energy source?

A

Some tissues such as cardiac muscle use fats as their preferred energy source. However, dietary carbohydrate is the most common source, although amino acids can also be used.

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

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6
Q

Structure of fatty acid

A
  • Fatty acid are chains of methyl groups with a carboxyl group at the end (terminal)
  • Fatty acids can be saturated with single bonds or unsaturated with double bonds
  • Humans unable to create double bonds in positions less than 9- these essential fatty acids must be obtained from diet
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7
Q

Example of saturated fatty acid

A

Palmitate

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8
Q

Example of unsaturated fatty acid

A

Oleate

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9
Q

How is lipid synthesis and degradation an example of compartmentalisation?

A

-Mostly occur in liver hepatocytes

Synthesis= occurs in the cytosol
Breakdown (beta oxidation)= occurs in the mitochondria

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10
Q

How are lipid synthesis and degradation regulated?

A

Reciprocally regulated

Synthesis during excess calorie intake and breakdown is inhibited

During breakdown then synthesis is inhibited

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11
Q

Structure of triglycerides

A

They are neutal fats- most fats are stored in this way

  • 3 fatty acids attached to a glycerol backbone
  • Stores of energy
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12
Q

How can glycerol be made?

A

Glycerol can be made from glycolysis by glycerol-3-phosphate, glycerol can also be fed into glycolysis at this point.

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13
Q

What is the starting block for the synthesis of fatty acid?

A

ACoA

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14
Q

How is fatty acids made from ACoA?

A

ACoA is converted into citrate in the Kreb cycle

Citrate is transported out of the mitochondria and into cytosol

ACoA then removed from citrate

This is converted into fatty acids

Fatty acids can remain in the liver (liver lipids) or be exported bound within lipoproteins or bound to albumin as free fatty acid (transported to peripheral tissue e.g. adipocytes for storage)

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15
Q

How can cholesterol be made?

A

From ACoA

Cholesterol is then transported to various tissues to be incorporated into membranes or for steroid synthesis

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16
Q

Where does fatty synthesis occur and what are the 3 substrates required?

A

It occurs in the cytosol.

Fatty acid synthesis requires:

  • Acetyl CoA
  • NADPH
  • ATP
17
Q

Explain the transfer of acetyl CoA to cytosol

A

This is done using the citrate-malate antiport

The process is cylindrical:

  • Citrate pumped into cytosol
  • Breaks down to give ACoA and oxaloacetate
  • Oxloacetate can be converted to malate which can be converted into pyruvate (NADPH produced in the last step)
  • Pyruvate is then transported back into mitochondrion and converted into oxaloacetate
  • This can combine with ACoA to Citrate thus completing the cycle
18
Q

Explain the first step of fatty acid synthesis

A
  • This is the rate limiting step
  • ACoA binds to acyl carrier protein (ACP)

Acetyl CoA + ATP + HCO3- –*—> Malonyl CoA + ADP + Pi

  • C2 to C3
  • Enzyme used is *Acetyl CoA carboxylase
  • Requires ATP and vitamin biotin

Positive feedback: Citrate (rise when flow of glucose through glycolytic pathway increases)

Negative feedback: Palmitate (end product of fatty acid synthesis)

19
Q

What regulates the enzyme Acetyl CoA carboxylase?

A
  • Inhibited by phosphorylation. Glucagon stimulates phosphorylation which therefore inhibits the enzyme.

ACoA carboxylase is increased by high carbohydrate and low fat

ACoA carboxylase is decreased by low carbohydrate and high fat

20
Q

Explain fatty acid synthesis - Elongation

A
  • C2 to C4

The first rate limiting step produces malonyl CoA that reacts with ACP (acyl carrier protein) to form Malonyl ACP (3C molecule)

Acetyl ACP and Malonyl ACP undergo a condensation reaction releasing CO2 producing Acetoactyl-ACP (4C molecule)

21
Q

What happens after elongation in the synthesis of fatty acids?

A

There are then three reactions that occur, a reduction, a dehydration and then another reduction coming out still as a 4C molecule of Butyryl-ACP.
The Butyryl ACP then reacts with a further Malonyl-ACP in a condensation reaction with the generation of a second CO2, now we have a 6-carbon molecule.

22
Q

Where does the NADPH come from in the synthesis of fatty acids?

A

It is either generated through the citrate-malate transporting or the pentose-phosphate pathway

23
Q

What is fatty acid synthase?

A

All the enzymes required for fatty acid synthesis form a multi-functional complex called fatty acid synthase which exists as an dimer.
By having a multi-enzyme complex all the reactions to occur are very close to each other and the products of one reaction are very close to the active site of the next enzyme in the chain.

24
Q

What is cholesterol and how is it transported?

A

It is a rigid hydrophobic molecule that is virtually insoluble in water. It is an important membrane component.

It is transported in the circulation as cholesteryl esters.

25
Q

What is cholesterol a precursor for?

A

Sterols
Steroids
Bile Salts

26
Q

Can cholesterol provide energy?

A

No

It cannot be oxidised to O2 and H2O

27
Q

Describe cholesterol synthesis

A
  • Mainly occurs in the ER
  • Over 30 steps
  • Starts with the activation of acetate to acetyl-CoA so cholesterol can be generated from a carbohydrate source similar to the synthesis of fatty acids
  • Target for therapeutic interventions: convertion of 3 hydroxyl-3-methylglutaryl CoA (HMGCoA) to mevalonate by HMGCoA reductase
28
Q

What inhibits HMGCoA reductase and what is the consequence of this?

A

Cholesterol inhibits HMGCoA reductase, the enzyme involved in its own synthesis

It is therefore difficult to reduce circulating cholesterol by diet alone as endogenous synthesis is increased. This problem therefore needs to be tackled by inhibiting the enzyme and diet.

29
Q

Explain fatty acid degradation

A

It is the release of energy from reserves stored in adipose tissue

Step 1: Mobilisation of fatty acid in adipocyte where it is transported back to the liver

Step 2: Activation of fatty acids in hepatocyte cytosol by acyl-CoA synthase

Step 3: The fatty acid is degraded in the liver mitochondria in the process called beta oxidation

30
Q

What is the liver’s main energy source?

A

Lipids/fatty acids

31
Q

Explain mobilisation of fatty acids

A
  • Stimulation of the 7TM G-protein coupled receptor by glucagon or adrenaline
  • cAMP activates PKA
  • Phosphorylation of triacylglycerol lipase which breaks down triacylglycerol to diacylglycerol
  • Diacylglycerol further acted upon by lipases leading to free fatty acids and glycerol which can diffuse through the plasma membrane leaving the adipocyte

This step is important when food is not readily available i.e. Starvation or excersize stimulated by glucagon and adrenaline but inhibited by insulin

32
Q

What is the fate of glycerol?

A

The glycerol is absorbed by the liver and can be converted back to glucose (gluconeogenesis) or converted to pyruvate (glycolysis)

33
Q

Explain activation of fatty acids

A

-Fatty acids are transported to the liver and activated by acyl-CoA synthase in the cytoplasm
- This gives Acyl-CoA by activation and it is then transported across the inner mitochondrial membrane (enzyme translocase) bound to the alcohol carnitine
’
Cartinine deficiency can cause muscle weakness or death

34
Q

What enzyme activates fatty acids in the hepatocyte cytoplasm?

A

Acyl-CoA synthase

35
Q

What inhibits the transportation of activated fatty acid (Acyl CoA) across inner mitochondrial membrane?

A

The transport is also inhibited by malonyl-CoA which is the first thing in the synthesis of fatty acids. So if it builds up, we will be moving towards synthesis so this degradation transport process is inhibited.

36
Q

Explain fatty acid oxidation (beta oxidation) which is step 3 of fatty acid degradation

A
  • occurs in liver mitochondria
  • Acyl-CoA degraded by removal of 2C units by B oxidation
  • FADH2, NADH and acetyl-CoA are produced
  • FADH2 and NADH form ATP
  • ACoA tend to be converted to ketone bodies but can also enter into CCA cycle (in presence glycolysis) and form ATP

There is cleaving of fatty acid until it reaches a certain chain length
Odd length: proprionyl CoA. Odd numbered double bonds are removed by isomerase

Even numbered double bonds are removed by reductase and isomerase

37
Q

Explain ketogenesis

A
  • ACoA –> Ketone bodies
  1. Acetyl-CoA from breakdown of fatty acids is converted to acetocacetyl-CoA
  2. Acetoacetyl-CoA is converted to HMG-CoA (by enzyme B-hydroxy-B-methyglutaryl-CoA)
  3. HMG-CoA converted to acetoacetate

The 3 ketone bodies: Acetoacetate can be reduced to 3-β-hydroxybuterate or non-enzymatically to acetone

The synthesis of ketone bodies are regulated by the insulin/glucagon ratio. Ketogenesis is high when the ratio is low as this inhibits acetyl-CoA carboxylase (rate limiting step in fatty acid synthesis).

38
Q

What is the fate of ketone bodies?

A

Acetoacetate is converted in the non-hepatic tissue back to acetyl-CoA, this can then be used to generate ATP.
Ketone bodies are a major energy source for cardiac muscle and renal cortex dependent on flow of carbohydrate in glycolysis (glucose is preferred).

During starvation or diabetes 75% of the brains energy is derived from acetoacetate – the production of ketones increases with decreased food intake.

39
Q

Explain hormonal regulation of fat metabolism

A

Insulin

  • Increases glycolysis
  • Increases fatty acid synthesis in the liver
  • Increases TG storage in adipose tissue
  • Decreases beta oxidation

Glucagon and Adrenaline

  • Increases TG mobilisation
  • Inhibits fatty acid synthesis

MCBHD- Molecular and Cellular Basis of Health and Disease (27 decks)

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