Fatty Acid Production and Oxidation Flashcards Preview

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Flashcards in Fatty Acid Production and Oxidation Deck (34):
1

Name the 3 main sites of lipogenesis

Liver, white adipose tissue and lactating mammary glands

2

Name the type of transport shuttle that is involved in lipogenesis

Carnitine shuttle

3

Name the type of transport shuttle that is involved in lipolysis

Citrate shuttle

4

What is malonyl-CoA and how does it affect lipolysis?

malonyl-CoA is an intermediate in the mechanism of fatty acid synthesis (lipogenesis) and it works to inhibit the carnitine shuttle of lipolysis to prevent newly formed fatty acids from being oxidised in the mitochondriia

5

What is the role of acetyl CoA carboxylase in lipogenesis?

Conversion of acetyl CoA to malonyl CoA

6

Describe how acetyl CoA carboxylase can be modified by polymerisation

Enzyme is activated when in polymerised, and inactive when not. Citrate activates this enzyme by promoting polymerisation (as a lot of citrate indicates a lot of glucose which may need conversion to fatty acids). Conversely, the enzyme is inhibited by the final product of fatty acid synthesis (palmitoyl-CoA) which causes depolymerisation of filaments.

7

Describe how acetyl CoA carboxylase can be modified by hormone-dependent phosphorylation

Glucagon activates cAMP-dependent protein kinase which phosphorylates enzyme and inactivates it. Insulin promotes dephosphorylation to activate enzyme and lipid synthesis.

8

Name the three ways in which acetyl CoA carboxylase activity can be modified

polymerisation, phosphorylation and long-term genetic control

9

Why is lipolysis necessary?

Carbohydrate stores can only provide short-term energy buffering, and other sources required in long-term starvation (e.g. lipids and ketone bodies)

10

What is the initial substrate of lipolysis?

Triacylglycerol (TAG)

11

What are the two products of lipolysis?

Glycerol and 3 free fatty acids

12

Describe what happens to the free fatty acids formed from lipolysis

can be oxidised for energy (in muscle/liver - oxidative tissues) to form acetyl CoA (enters TCA cycle) in addition to many molecules of FADH2 and NADH which enter ETC. Fatty acids could also be converted to ketone bodies in liver for use in non-oxidative tissues (brain and erythrocytes)

13

Describe what happens to the glycerol formed in lipolysis

Can be use for glucose synthesis in liver or phosphorylated to form PEP to be used in glycolysis or gluconeogenesis

14

What is the role of the hormone-sensitive lipase in lipolysis?

Converts triacylglycerol into glycerol and 3 free fatty acids

15

Describe how the hormone-sensitive lipase enzyme is regulated

Sensitive to cAMP levels (which respond to hormone signals). Glucagon/adrenaline stimulates enzyme to encourage glycerol and FFA production. Insulin inhibits the enzyme in order to inhibit further production of glucose as it's not required.

16

Describe the process of fatty acid activation in lipolysis

In liver/muscle cells: outer mitochondrial membrane facilitates free fatty acids to combine with CoA in presence of thiokinase to produce activated acyl CoA

17

Describe the carnitine shuttle in lipolysis

acyl CoA attaches to carnitine and loses CoA group in the presence of CPT-I. Fatty acyl-carnitine is formed and transported across membrane into mitochondrial matrix by translocase enzyme. Fatty acyl group transferred back to CoA (fatty acyl carnitine + CoA -> carnitine + fatty acyl CoA) using enzyme CPT-II. Carnitine is then returned to outer mitochondrial membrane to exchange for another molecule of fatty acyl-carnitine

18

What is meant by the 'carnitine shuttle'?

CPT-I, CPT-II and translocase enzymes involved in the transport of acyl CoA into the mitochondrial matrix in fatty acid breakdown

19

What is malonyl-CoA?

Compound formed in fatty acid synthesis

20

Describe three ways in which the activity of the CPT-I enzyme (in the carnitine shuttle) can be modulated

Stimulated by glucagon (via cAMP), regulated transcriptionally with activity rising in extended fasting and diabetes (to increase fatty acid oxidation) and malonyl-CoA inhibits enzyme to prevent newly formed fatty acids from being oxidised immediately in the mitochondrial matrix

21

Which two types of cell cannot undergo beta-oxidation of fatty acids, and why?

Brain cells and erythrocytes as they do not have mitochondria

22

How to we obtain energy from fatty acids?

through beta oxidation; this involves oxidation by acetyl CoA dehydrogenases in the mitochondrial matrix

23

What are the products of beta oxidation of fatty acids?

NAD, FADH2 and acetyl-CoA. The first two will enter the ETC directly to release energy, whereas the acetyl CoA will enter the TCA cycle to release energy.

24

Define 'ketogenesis'

The formation of ketone bodies from acetyl CoA (produced from the beta oxidation of fatty acids)

25

Where does ketogenesis occur?

Mitochondria of liver cells

26

Name the 4 enzymes involved in ketogenesis

acetoacetyl CoA thiolase, HMG-CoA synthase, HMG-CoA lyase, 3-hydroxybutyrate dehydrogenase

27

Describe the mechanism of ketogenesis

1) Two acetyl CoA molecules (from B-oxidation of fatty acids) converted to acetoacetyl CoA via acetoacetyl CoA thiolase enzyme.
2)This molecule is then converted to HMG-CoA in presence of HMG-CoA synthase enzyme
3) HMG-CoA converted to acetoacetate in presence of HMG-CoA lyase enzyme
4) Acetoacetate split into two types; spontaneous reaction forms acetone in decarboxylation reaction, or 3-hydroxybutyrate is formed in the presence of a dehydrogenase enzyme

28

How does acetylation affect the HMG-synthase enzyme?

acetylation deactivates enzyme

29

Name the 3 main structures where ketone bodies are utilised

Heart (preferentially over glucose), brain and muscle

30

How does the brain respond to starvation metabolically?

Instead of using 100% glucose, begins to use 50% ketone bodies to conserve glucose when glycogen stores are low

31

Why can't the liver oxidise ketone bodies?

Does not have the 3-ketoacetyl CoA transferase enzyme and therefore it cannot activate the acetoacetate in the oxidative pathway

32

Describe the effects of excessive ketone body production

If formation far greater than use, hydrogen ions will accumulate leading to ketoacidosis as this exceeds buffering capacity of blood.

33

Why are individuals with uncontrolled diabetes at risk of ketoacidosis?

Insulin normally inhibits ketone body production

34

How does the oxidation of glucose affect the oxidation of lipid?

If there is high glucose, then the levels of citrate will rise as a lot of aerobic respiration will be occurring; this citrate will be converted to malonyl-CoA which will go on to inhibit the carnitine shuttle of fatty acid oxidation, and therefore high glucose levels inhibit fatty acid breakdown when it's not necessary