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

(LUSUMA) Metabolism, Endocrinology & Haematology > S2) Energy Production III — Lipids, β-Oxidation & Ketone Bodies > Flashcards

Flashcards in S2) Energy Production III — Lipids, β-Oxidation & Ketone Bodies Deck (34)
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1

Identify and describe the three different classes of lipids

- Fatty acid derivatives – fatty acids and triacylglycerol

Hydroxy-methyl-glutaric acid derivatives – ketone bodies, cholesterol

- Vitamins – ADEK

2

Explain how energy storage varies between a healthy and obese man

3

Describe the structure of triacyglycerol

Triacylglycerols are hydrophobic

4

Describe the storage of TAG

- Stored in an anhydrous form

- Stored in adipose tissue

- Storage / mobilisation under hormonal control 

5

Identify three circumstances where triacylglycerols are used

- Prolonged exercise

- Starvation 

- Pregnancy 

6

Identify the tissues involved in triglyceride metabolism and illustrate their role

7

Where does stage 1 of TAG metabolism occur?

Gastrointestinal tract (extracellular)

8

What occurs in stage 1 of TAG metabolism?

- Extracellular hydrolysis of dietary lipids (TAG) in small intestine by pancreatic lipases

- Fatty acids and glycerol are formed

9

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

⇒ Converted back to triglycerides in GI tract

⇒ Packaged into lipoprotein particle (chylomicrons)

⇒ Released into circulation via lymphatics

⇒ Carried to adipose tissue

⇒ Stored as triglyceride

10

Describe fat mobilisation

- Fatty acids are released when needed

- They are carried to tissues as albumin-fatty acid complex 

11

Fat mobilisation is under hormonal control.

Describe this

Hormone-sensitive lipase:

- Increases with glucagon/adrenaline

- Decreases with insulin 

12

Which consumer tissues are fatty acids not mobilised to?

- Cells without mitochondria e.g. RBC

- Brain; fatty acids do not easily pass blood-brain barrier 

13

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

1 – Glucose transport

2 – Glycolysis

3 – Esterification

4 – Lysis

5 – Re-esterification 

14

What causes the release of fatty acids as alternative fuel?

Low extracellular [glucose] 

15

Describe the molecular structure of fatty acids

Amphipathic: contain hydrophilic & hydrophobic groups

16

What are the two types of fatty acids?

- Saturated: no double bonds between neighbouring C-atoms

- Unsaturated: 1/more double bonds between neighbouring C-atoms

17

Where does stage 2 of fatty acid metabolism occur?

Mitochondrion

18

In three steps, describe what occurs in fatty acid catabolism

⇒ 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

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

Describe how this occurs

- 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

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

Describe how and why this process is regulated

- Regulated, so controls the rate of FA oxidation

- Inhibited by malonyl~CoA (biosynthetic intermediate)

21

Fatty acid catabolism is also called β oxidation. 

Identify three key features of this process

- H+ and e- transferred to NAD+ and FAD

- Stops in absence of O2

- No ATP synthesis 

22

Briefly describe glycerol metabolism

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

23

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

What is its function?

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

24

Three ketone bodies are produced in the body. 

What are they?

- Acetoacetate: CH3COCH2COO- (liver)

- Acetone: CH3COCH3

- β-hydroxybutyrate: CH3CHOHCH2COO(liver) 

25

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

- Normal < 1 mM

- Starvation = 2-10 mM (physiological ketosis)

- Untreated Type 1 diabetes > 10 mM (pathological ketosis) 

26

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

27

How is acetone formed?

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

28

Explain how ketone body production is controlled in the liver 

29

Outline the pathways involved in ketone metabolism

30

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

- 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