S2) Energy Production III — Lipids, β-Oxidation & Ketone Bodies Flashcards

1
Q

Identify and describe the three different classes of lipids

A
  • Fatty acid derivatives – fatty acids and triacylglycerol
  • Hydroxy-methyl-glutaric acid derivatives – ketone bodies, cholesterol
  • Vitamins – ADEK
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2
Q

Explain how energy storage varies between a healthy and obese man

A
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3
Q

Describe the structure of triacyglycerol

A

Triacylglycerols are hydrophobic

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4
Q

Describe the storage of TAG

A
  • Stored in an anhydrous form
  • Stored in adipose tissue
  • Storage / mobilisation under hormonal control
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5
Q

Identify three circumstances where triacylglycerols are used

A
  • Prolonged exercise
  • Starvation
  • Pregnancy
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6
Q

Identify the tissues involved in triglyceride metabolism and illustrate their role

A
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7
Q

Where does stage 1 of TAG metabolism occur?

A

Gastrointestinal tract (extracellular)

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8
Q

What occurs in stage 1 of TAG metabolism?

A
  • Extracellular hydrolysis of dietary lipids (TAG) in small intestine by pancreatic lipases
  • Fatty acids and glycerol are formed
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9
Q

In 5 steps, describe what happens in TAG metabolism after absorption in to the GI tract

A

⇒ Converted back to triglycerides in GI tract

⇒ Packaged into lipoprotein particle (chylomicrons)

⇒ Released into circulation via lymphatics

⇒ Carried to adipose tissue

⇒ Stored as triglyceride

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10
Q

Describe fat mobilisation

A
  • Fatty acids are released when needed
  • They are carried to tissues as albumin-fatty acid complex
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11
Q

Fat mobilisation is under hormonal control.

Describe this

A

Hormone-sensitive lipase:

  • Increases with glucagon/adrenaline
  • Decreases with insulin
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12
Q

Which consumer tissues are fatty acids not mobilised to?

A
  • Cells without mitochondria e.g. RBC
  • Brain; fatty acids do not easily pass blood-brain barrier
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13
Q

In 5 steps, describe and illustrate the triglyceride/fatty acid cycle in adipose tissue

A

1 – Glucose transport

2 – Glycolysis

3 – Esterification

4 – Lysis

5 – Re-esterification

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14
Q

What causes the release of fatty acids as alternative fuel?

A

Low extracellular [glucose]

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15
Q

Describe the molecular structure of fatty acids

A

Amphipathic: contain hydrophilic & hydrophobic groups

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16
Q

What are the two types of fatty acids?

A
  • Saturated: no double bonds between neighbouring C-atoms
  • Unsaturated: 1/more double bonds between neighbouring C-atoms
17
Q

Where does stage 2 of fatty acid metabolism occur?

A

Mitochondrion

18
Q

In three steps, describe what occurs in fatty acid catabolism

A

⇒ FA is activated outside the mitochondrion

⇒ FA is transported across the inner mitochondrial membrane using a carnitine shuttle

⇒ FA cycles through sequence of oxidative reactions, with C2 removed each cycle

19
Q

Fatty acid activation occurs outside the mitochondria, in the cytoplasm.

Describe how this occurs

A
  • Activated by linking to coenzyme A by the action of fatty acyl CoA synthase
  • Activated fatty acids (fatty acyl~CoA) do not readily cross the inner mitochondrial membrane (carnitine shuttle)
20
Q

Carnitine shuttle transports fatty acyl~CoA across the mitochondrial membrane.

Describe how and why this process is regulated

A
  • Regulated, so controls the rate of FA oxidation
  • Inhibited by malonyl~CoA (biosynthetic intermediate)
21
Q

Fatty acid catabolism is also called β oxidation.

Identify three key features of this process

A
  • H+ and e- transferred to NAD+ and FAD
  • Stops in absence of O2
  • No ATP synthesis
22
Q

Briefly describe glycerol metabolism

A

Glycerol can be transported in the blood to the liver, where it is metabolised

23
Q

Acetyl-CoA is the main convergence point for catabolic pathways.

What is its function?

A

Acetyl~CoA is the most important intermediate in both catabolic and anabolic pathways

24
Q

Three ketone bodies are produced in the body.

What are they?

A
  • Acetoacetate: CH3COCH2COO- (liver)
  • Acetone: CH3COCH3
  • β-hydroxybutyrate: CH3CHOHCH2COO- (liver)
25
Q

Describe the physiological and pathological variation in the plasma concentration of ketone bodies

A
  • Normal < 1 mM
  • Starvation = 2-10 mM (physiological ketosis)
  • Untreated Type 1 diabetes > 10 mM (pathological ketosis)
26
Q

Briefly outline the pathways in which ketone bodies are synthesised by liver mitochondria

A
27
Q

How is acetone formed?

A

Acetone is formed from the spontaneous (non-enzymatic) decarboxylation of acetoacetate

28
Q

Explain how ketone body production is controlled in the liver

A
29
Q

Outline the pathways involved in ketone metabolism

A
30
Q

Explain how ketone bodies synthesis is regulated by the insulin:glucagon ratio in fed and starvation states

A
  • Fed state: high insulin:glucagon inhibits lyase and activates reductase → cholesterol synthesis
  • Starvation state: low insulin:glucagon inhibits reductase and activates lyase → ketone body synthesis
31
Q

Illustrate how ketone bodies spare glucose in early starvation/diabetes

A
32
Q

Illustrate how ketone bodies spare glucose in late starvation/diabetes

A
33
Q

How are excess ketone bodies excreted from the body?

A

Above renal threshold, excreted in urine (ketonuria)

34
Q

How is acetone excreted from the body?

A

Volatile acetone may be excreted via the lungs (characteristic smell of acetone on breath)