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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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


Explain how energy storage varies between a healthy and obese man


Describe the structure of triacyglycerol

Triacylglycerols are hydrophobic


Describe the storage of TAG

- Stored in an anhydrous form

- Stored in adipose tissue

- Storage / mobilisation under hormonal control 


Identify three circumstances where triacylglycerols are used

- Prolonged exercise

- Starvation 

- Pregnancy 


Identify the tissues involved in triglyceride metabolism and illustrate their role


Where does stage 1 of TAG metabolism occur?

Gastrointestinal tract (extracellular)


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


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


Describe fat mobilisation

- Fatty acids are released when needed

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


Fat mobilisation is under hormonal control.

Describe this

Hormone-sensitive lipase:

- Increases with glucagon/adrenaline

- Decreases with insulin 


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 


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 


What causes the release of fatty acids as alternative fuel?

Low extracellular [glucose] 


Describe the molecular structure of fatty acids

Amphipathic: contain hydrophilic & hydrophobic groups


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


Where does stage 2 of fatty acid metabolism occur?



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 


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)


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)


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 


Briefly describe glycerol metabolism

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


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


Three ketone bodies are produced in the body. 

What are they?

- Acetoacetate: CH3COCH2COO- (liver)

- Acetone: CH3COCH3

- β-hydroxybutyrate: CH3CHOHCH2COO(liver) 


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) 


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


How is acetone formed?

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


Explain how ketone body production is controlled in the liver 


Outline the pathways involved in ketone metabolism


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