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Metabolism > Fats II- Ketogenesis and Cholesterol Synthesis > Flashcards

Fats II- Ketogenesis and Cholesterol Synthesis Flashcards

1
Q

Before oxidation, what enzyme activates fatty acids and links them to coenzyme A?

A

Thiokinase enzyme

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2
Q

What is the process by which fats can be fully oxidised to ATP?

A

β-oxidation produces Acetyl Co-A

- Can be converted into ATP or ketone bodies

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3
Q

How are ketone bodies used for energy?

A
  • Sent to bloodstream and travels to tissues NOT the liver

- Converted to Acetyl CoA

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4
Q

Where is the only place gluconeogenesis occurs?

A

Liver

- The only organ that can make glucose

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5
Q

What process provides fatty acids for oxidation and energy production?

A

Lipolysis

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6
Q

What substance may the body draw on for substrates of essential proteins and carbon for gluconeogenesis in a state of fasting and starvation?

A

Muscle protein

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7
Q

What are the useful products of β oxidation?

A
  • Acetyl CoA

- FADH2 and NADH

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8
Q

What is driving ketogenesis during fasting/starvation?

A
  • β-oxidation drives Acetyl CoA
  • Intermediates originally provided by amino acid oxidation are removed from TCA cycle are used for gluconeogenesis
  • Insufficient oxaloacetate to drive TCA cycle and use up acetyl CoA molecules from β-oxidation
  • Excess Acetyl CoA accumulates which undergoes ketogenesis
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9
Q

What does the liver need to continue β-oxidation?

A

Free coenzyme A

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10
Q

Where is the only place that ketone body synthesis takes place?

A

Mitochondrial matrix

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11
Q

What are the three ketone bodies that acetyl CoA can be converted to?

A
  • Acetoacetate
  • β-hydroxybutyrate
  • Acetone
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12
Q

What are ketone bodies converted to serve as an energy source?

A
  • Acetyl CoA
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13
Q

Which ketone bodies are more common?

A
  • Acetoacetate

- β-hydroxybutyrate

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14
Q

What happens to ketone bodies when they are not being used?

A

Acetone

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15
Q

What are the two key enzymes in ketogenesis from Acetyl CoA?

A
  • HMG-CoA synthase
  • HMG-CoA lyase
    (unique to hepatocytes)
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16
Q

How is acetone excreted?

A

Via urine or lungs

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17
Q

What do two acetyl CoA molecules produce?

A
  • Acetoacetyl CoA

- One co-enzyme A molecule is released and used in β-oxidation

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18
Q

What happens to acetoacetyl CoA after it is produced?

A
  • Reacts with another acetyl CoA

- Produces HMG CoA (essential intermediate)

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19
Q

What enzyme catalyses the reaction between Acetoacetyl CoA and Acetyl CoA?

A

HMG CoA synthase

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20
Q

What is HMG CoA converted to in ketogenesis?

A

Acetoacetate

21
Q

What enzyme catalyses the reaction converting HMG-CoA to acetoacetate?

A

HMG-CoA lyase

22
Q

What is Acetoacetate converted to in ketogenesis and what enzyme catalyses this?

A
  • β-hydroxybutyrate
  • β-hydroxybutyrate dehydrogenase
  • NADH + H+ -> NAD+
23
Q

What is detectable on a diabetic’s breath as a sign that they are undergoing ketogenesis?

A

Acetone

- Both acetoacetate and β-hydroxybutyrate

24
Q

Describe the fate of ketone bodies

A
  • Synthesised in the liver
  • Conversion back to Acetyl CoA
  • Oxidation in the TCA cycle in other tissues
  • Occurs in muscle and the brain during starvation
25
Q

Briefly describe type 1 diabetes mellitus

A
  • Elevated blood glucose results from inadequate secretion of insulin by islets of Langerhans in the pancreas
26
Q

Briefly describe type 2 diabetes mellitus

A
  • Shortage of insulin receptors- desensitisation to them
27
Q

What happens to glucose transport in diabetes mellitus?

A
  • Transport of glucose into muscle, liver and adipose tissue is significantly reduced
  • Cells are metabolically starved
28
Q

What happens to oxaloacetate in diabetes mellitus?

A
  • Increased gluconeogenesis consumes most of the available oxaloacetate
29
Q

What is an indication of high plasma levels of ketone bodies?

A
  • Acetone detected on the breath of type 1 diabetics
30
Q

What is the blood-brain barrier’s permeability to ketone bodies dependent on?

A

Monocarboxylic acid transporters (MCT-1)

31
Q

What increases the number of MCT1 transporters in the blood-brain barrier?

A
  • Fasting
32
Q

How can we tell that the only essential role of ketone bodies is as an alternative fuel for illness/long-term fasting?

A
  • Most patients with inborn errors involving ketogenesis develop normally
33
Q

What does imaging show as a symptom of HMG-CoA lyase deficiency?

A
  • Imaging generally shows asymptomatic white-matter abnormalities
34
Q

In what case would a ketogenic diet be effective?

A
  • In those who have a GLUT-1 deficiency
  • Where a high glucose diet may not be useful
  • Also successful treatment for patients with intractable epilepsy
35
Q

Describe the ketogenic diet

A
  • High in fat, moderate protein, low carbohydrate
  • Treatment for those whose tissues cannot access or properly process carbohydrates (like in pyruvate dehydrogenase deficiency)
36
Q

What is cholesterol?

A

A major class of lipid used in the body

37
Q

What are the functions of cholesterol?

A
  • Structural component of cell membranes- confers fluidity and regulates permeability
  • Substrate for synthesis of sex hormone, vitamin D and bile acids
38
Q

What is cholesterol mainly composed of?

A
  • Carbon and hydrogen
  • And solitary hydroxyl group attached to C3
  • Almost completely saturate one double bond at C5=C6
  • Mainly hydrophobic
39
Q

Where is cholesterol synthesised?

A
  • Liver is the main site
40
Q

Where can cholesterol be obtained in the diet?

A
  • Animal fat
41
Q

What is the rate limiting regulatory enzyme for cholesterol biosynthesis?

A
  • HMG- CoA reductase
42
Q

What enzyme is cholesterol synthesis is a target of statins (drugs)?

A

HMG-CoA reductase

43
Q

Describe the synthesis of cholesterol

A
  • 2 Acetyl CoA produce AcetoacetylCoA
    • CoA used in β-oxidation
  • Acetoacetyl CoA converted to HMG-CoA using enzyme HMG-CoA synthase
  • -CoA byproduct used in β-oxidation
  • HMG-CoA converted to Mevalonate which is then converted to Lanosterol
    • Both reactions use HMG-CoA reductase
  • Lanosterol converted to cholesterols
44
Q

What inhibits HMG-CoA reductase in a negative feedback loop?

A
  • Cholesterol
45
Q

What happens when statins inhibit HMG-CoA reductase?

A
  • Lowers levels of endogenously synthesised cholesterol
  • Stimulates increased LDL receptor expression in order to extract more cholesterol from blood
  • Lowers plasma cholesterol and risk of MI
46
Q

What do fungal cells convert lanosterol to?

A
  • Ergosterol
47
Q

What is ergosterol?

A
  • Important component of fungal cell membranes and not animal cell
  • Useful drug target
48
Q

What are examples of anti-fungals that inhibit enzymes necessary for ergosterol generation?

A
  • Terbinafine

- Imidazole

Metabolism (9 decks)

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