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MCBG > MCBG S18 Lipids > Flashcards

MCBG S18 Lipids Flashcards

1
Q

What are the 3 classes of lipids?

A

Fatty acid derivatives

Hydroxy-methyl-glutamic acids derivatives

Vitamins A,D,E and K.

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2
Q

Give 4 specific FA derivatives and their uses.

A

FAs - fuel
TAGs - fuel storage and insulation
Phospholipids - membrane and lipoproteins
Eicosanoids - paracrine signalling molecules.

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3
Q

Give 4 HMG derivatives and their uses.

A
  • Ketone bodies - water soluble fuel molecules.
  • Cholesterol - membrane and steroid hormone synthesis
  • Cholesterol esters - cholesterol Storage
  • Bile acids and salts - lipid digestion
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4
Q

Are TAGs hydrophobic or phillic?

In what form are they stored and where?

When are they utilised?

What type of control is their mobilisation and storage under?

A

Hydrophilic

Anhydrous - adipose tissue

Pregnancy, prolonged exercise, starvation

Hormonal

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5
Q

What’s are dietary TAGs transported around in the blood as?

What are the 2 places they will be transported to and why?

A

Chylomicrons

Adipose - storage
Consumer tissues - B-oxidation to release energy.

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6
Q

What type of enzyme will mobilise TAGs and in what form will they be carried to tissues as?

What hormones stimulate fat mobilisation and deposition?

A

Hormone sensitive lipases
Carried as albumin-FA complexes

Glucagon and adrenaline - mobilisation
Insulin - deposition

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7
Q

Why are RBCs and the brain not consumer tissues of FAs?

A

RBCs no mitochondria

FAs cant cross BBB easily.

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8
Q

Describe the fatty acid cycle in adipose tissue.

A

Glucose transported into cell enters glycolysis.
Converted to glycerol-1-P and combined with fatty acyl CoA converted into TAG by esterification
TAG lyses into glycerol and fatty acid.
Glycerol released into blood.
Fatty acid back to form fatty acyl CoA which will rejoin with re-esterify with glycerol-1-P.

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9
Q

How does decreased glucose concentration cause FA acid release from adipose?

A

Reduced glucose means glycerol-1-phosphate levels fall.

TAG can’t be made and as a result TAG dissociation will cause fatty acids to enter circulation as albumin-FA complexes.

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10
Q

Before a FA may be metabolised it must go through FA activation.

What does this involve and what enzyme is involved?

A

FA + CoA + ATP -> FACoA + AMP + 2Pi

Fatty acyl CoA synthase

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11
Q

Activated FAs can not cross the inner mitochondrial membrane.

Describe the mechanism by which they enter the mitochondria.

A

Cartinine shuttle

FA-CoA donates FA to carntine by action of enzyme carnitine acyl transferase 1 (CAT1)
Acyl carnitine is then transported into the mitochondria where CAT 2 will transfer the FA to another CoA will bind to it reforming FA-CoA inside. Carnitine gets transported back through to the other side.

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12
Q

What is the carnitine shuttle regulated by?

What can defects in this system lead to?

A

Malonyl CoA

Exercise intolerance
Lipid droplets in muscle due to decreased FA metabolism.

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13
Q

Describe the overall of B-oxidation.

What is made?

What is used up?

What is the fate of the end product?

A

FA cycles through a sequence of oxidative reactions with 2C being removed each cycle.

FADH2 and NADH are made and H20 is used up.

Each 2C binds with Acetyl CoA and enters TCA.

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14
Q

Is B-oxidation aerobic or anaerobic?

Does it involved substrate level phosphorylation?

A

Aerobic

No SLP

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15
Q

Describe the process glycerol metabolism.

How can glycerol be stored?

A

Glycerol phosphorylated by glycerol kinase to glycerol phosphate.

Glycerol phosphate dehydrogenated to DHAP which can enter glycolysis.

Glycerol phosphate can also enter TAG cycle for storage in adipose tissue.

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16
Q

Acetyl CoA is the ______ point for many pathways.

CoA contains vitamin ___ aka __________ _____.

A

Convergence
B5
Pathenoic acid.

17
Q

What are 3 routes Acetyl CoA can take?

A

Enter TCA - 2CO2

Converted to FAs - TAG / phospholipid synthesis

Made into hydroxymethylglutaric acid.
- Ketone bodies or cholesterol - from cholesterol to steroid hormones.

18
Q

What is ketogenesis?

A

Production of ketone bodies by the break down of FAs and ketogneic amino acids.

19
Q

What are the 3 types of ketone bodies?

Where are they made?

A

Acetoacetate
B-hydroxybutryate
Made in liver

Acetone - spontaneous break down of acetoacetate.

20
Q

What is the normal ketone body concentration of ketone bodies?

What is the [ketone bodies] during starvation and what is this state called?

What is the [ketone bodies] in untreated type 1 diabetes and what is this state called?

A

<1mM

2-10mM - Physiological ketosis.

> 10mM - Pathological ketosis

21
Q

Describe the process of ketogenesis.

A

Acetyl CoA converted to HMG-CoA
HMG-CoA converted by HMG-CoA lease to acetoacetate.
Acetoacetate can be reduced to B-hydroxybutyrate or spontaneously decarboxylates to acetone.

22
Q

HMG-CoA may be converted to another intermediate that is not acetoacetate.

Describe this process and purpose of it.

What inhibits this process and what is the clinical significance of this?

A

HMG-CoA converted to mevalonate by HMG-CoA reductase.

Mevalonate converted to cholesterol.

Statin drugs inhibit HMG-CoA reductase.
Reduce blood cholesterol.

23
Q

Describe the control of ketone production.

A

When [glucose] low FAs mobilised.
B-oxidation of FAs - Acetyl CoA.
B-oxidation uses up NAD+.
Low substrate availability of Isocitrate dehydrogenase and a-ketaglutarate dehydrogenase.
Citrate builds up and oxaloacetate levels go down.
Acetyl-CoA diverted to ketogenesis pathway.

24
Q

Describe the process of ketone body metabolism.

A

Acetoacetate and hydroxybutyrate travel to respiring tissues ie brain and muscle.
Acetoacetate combine with CoA to form acetoacetylCoA.
- CoA derived from TCA succinyl CoA step.
B-hydroxybutyrate must get oxidised to acetoacetate prior to same process.
- NADH made
AcetoacetylCoA made into AcetylCoA and enters TCA.

25
Q

When body is in fed state, aka insulin:glucagon ratio is high, what regulation of ketone body synthesis occurs?

A

Inhibition of HMG-CoA lyase.
HMG-CoA builds up.
Increased activity of HMG-CoA reductase pathway which ultimately leads to increased levels of cholesterol.

26
Q

When body is in starvation state,aka low insulin:glucagon, what regulation of ketone body synthesis occurs?

A

Stimulation of lyase.
More HMG-CoA -> acetoacetate,
Inhibition of HMG-CoA reductase also occurs.

27
Q

The brain can use ketone bodies, but under starvation why are ketone bodies made?

A

The brain has a base requirement for glucose.
Therefore ketone bodies can be used as alternative fuel for muscle and other tissues which the brain can use the circulating glucose.

28
Q

Are ketone bodies water soluble?

At what concentration of ketone bodies is the renal threshold surpassed?

What can increased levels of acetoacetate and B-hydroxybutyrate lead to and why?

A

Yes
10mM
Ketoacidosis - they are relatively strong acids.

29
Q

Acetone is volatile.

This means during times of starvation what can be observed?

A

Fruity smell on breath because volatile acetone is excreted by the lungs.

MCBG (9 decks)

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