Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

02 - MCBG > 10 - Lipid and Ketone Body Metabolism > Flashcards

10 - Lipid and Ketone Body Metabolism Flashcards

1
Q

What is the general structure of a lipid?

A
  • Diverse, contain C,H and O and sometimes P, N
  • More reduced than carbohydrates
  • Not water soluble
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the three classes of lipids?

A

Fatty acid derivatives:

  • FA = fuel molecule - TAG = storage molecule
  • Phospholipids - Eicosanoids (local mediators)

Hydroxy-methylglutaric acid derivatives:

  • Ketone bodies (C4 - water soluble)
  • Cholesterol - Cholesterol esters (storage)
  • Bile acid and salts

Vitamins:

A,D,E,K essential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is TAG synthesised and broken down?

A
  • Under hormonal control to be stored in adipose anhydrously as hydrophobic.

Esterification: Insulin

Lipolysis: Glucagon, Cortisol, Adrenaline, GH

Lipolysis during starvation, pregnancy and prolonged exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are triacylglycerols metabolised extracellularly?

A
  • Hydrolysed by pancreatic lipase in SI. Requires bile salts
  • Produce FA and Glycerol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where does B-oxidation not occur?

A
  • RBC as no mitochondria
  • Brain as FA can’t pass blood-brain barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens to glycerol when it has been produced from TAG metabolism?

A

Goes through blood to liver where it is stored or metabolised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens to FA when they have been digested from TAG?

A
  • Converted back to TAG in G.I
  • Packaged into lipoproteins called chylomicrons
  • Released into circulation by lymphatics and carried to adipose tissue to be stored
  • Released by hormone-sensitive lipase
  • Carried to consumer tissues by albumin - FA complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How are fatty acids held in adipose tissue?

A
  • When glucose conc decreases, insufficient glycerol-1-phosphate so fatty acyl-coA cant be converted so FA builds up due to backlog and is released
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is B-oxidation?

A

Oxidation of fatty acids to release energy, in the mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two properties of fatty acids?

A
  • Amphipathic
  • Saturated/Unsaturated (linolenic acid essential as can’t introduce C double bond after C9)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are fatty acids catabolised?

A
  • Activated by linking to CoA outside the mitochondria
  • Transported via carnitine shuttle through inner mitochondrial membrane as activated FA do not readily cross inner membrane
  • Series of oxidative reactions with C2 removed each time and NADH and FADH2 being produced each time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How are fatty acids activated?

A

Fatty acyl CoA synthase links FA to CoA, using ATP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does fatty-acyl CoA get across inner mitochondrial membrane?

A
  • On it’s own cant get across membrane so CAT 1 (carnitine acyltransferase) removes CoA and adds carnitine to produce acyl carnitine
  • Acyl carnitine shuttles across carnitine shuttle transporter into mitochondria
  • CAT2 adds CoA back and removes carnitine which shuttles back over.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is carnatine shuttle transporter regulated?

A
  • Controls rate of FA oxidation
  • CAT inhibited by biosynthetic intermediate malonyl CoA
  • If dect in CAT, will lead to lipid droplets in abnormal places as lipids can’t be broken down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain key points of B-oxidation?

A
  • Cycle removing 2C each time
  • Oxidation
  • Produces NADH and FADH2
  • Needs O2
  • No ATP synthesis
  • Greater yield than glucose as more turns of TCA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is acetyl coA the convergance point of catabolic pathways?

A
  • Acetyl (CH3CO) linked to CoA by S bond
  • High energy when hydrolysed so acetyl is activated
  • CoaA made of Vitamin B5
17
Q

Why can’t glucose be made by reversing glycolysis of pyruvate?

A

Some irreversible reactions, have to bypass these steps using other routes

18
Q

How is acetyl CoA produced and how does it synthesise lipids?

A
  • Catabolism of FA, sugars, alcohol and AA
  • In liver lipids synthesised. 2 CoA makes FA, 3 CoA makes HMG
19
Q

What are the three main ketone bodies and their functions?

A
  • Acetoacetate, B-Hydroxybutyrate, Acetone (breakdown of acetoacetate)

Used as an alternative fuel source to glucose in starvation. Acetone excreted

20
Q

Where are ketone bodies produced and what are normal levels?

A

Ketone bodies are synthesised in liver mitochondria from acetyl~CoA by a pathway that produces hydroxymethyl glutaryl CoA (HMG CoA). This is converted to acetoacetate by a lyase enzyme These enzymes are regulated by hormones

  • <1mM normal
  • 2-10mM starvation
  • >10mM untreated type 1 diabetes (fruit breath)
21
Q

What is ketone body production regulated by?

A

Insulin to Glucagon ratio.

  • Low ratio, lyase activated and reductase inhibited
  • High ratio , reductase activated and lyase inhibited
22
Q

What do statins do?

A

They inhibit the enzyme that converts HMG-CoA into cholesterol

23
Q

Why are ketone bodies synthesised?

A
  • Alternative source of energy during starvation to allow there to still be some glucose for cerebal activity
  • Used by all tissues that contain mitochondria, even CNS
  • Converted to CoA so can enter TCA
24
Q

What is the general process of ketogenesis during early starvation?

A
  • Low glucose
  • FA released by lipolysis in adipose
  • Travel to liver by blood
  • Ketoneogenesis (as high NADH from fatty acids being converted to acetyl coA so signals inhibits TCA enzymes isocitrate dehydrogense and a-ketoglutarate dehydrogenase, so acetyl coA forced down ketone route)
  • KB travel by blood to tissue and are utilised to form acetyl CoA
  • Enter TCA
25
Q

What is the process during late starvation?

A
  • Adipose stores mobilised for keton bodies to supply energy for rest of body
  • Proteins in muscle broken down to aa for gluconeogenesis in liver for glucose for brain
  • Glycogenolysis in liver for basal glucose
26
Q

Why can ketones travel in the blood?

A

They are water soluble

27
Q

What is ketonuria?

A

Ketones in urine due to ketone body levels above renal threshhold

28
Q

What is ketoacidosis?

A
  • Ketone bodies are strong organic acids and are dissolved in blood. Large concentrations of them in the blood mean buffering system cant deal with them so lower pH
  • Acetone can be excreted via lungs so can smell it on breath
  • Likely to occur in untreated type 1 diabetes
29
Q

What does ketogenesis rely on?

A
  • Insulin:Glucagon plasma ratio
  • Fatty acid substrate in liver from lipolysis in adipose
30
Q

What is coenzyme A derived from?

A

Vitamin B5

31
Q

Why do fatty acids release more energy than glucose?

A

The break down of lipids by beta-oxidation causes more acetyl CoA to be formed, e.g 9, so more turns of the TCA and more reducing power produced

32
Q

How do ketone bodies join the TCA cycle?

A
33
Q

Discuss all 4 stages of catabolism for protein, carbohydrates, lipids (TAGS) and alcohol.

A

02 - MCBG (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions