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Biochemistry > Lipoprotein handeling > Flashcards

Lipoprotein handeling Flashcards

1
Q

What are the different forms of fatty acids?

A

Triglycerides (90%), cholesterol, cholesterol esters, phospholipids, free fatty acids

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2
Q

Which forms of fatty acid is hydrophobic? What is the consequence of this?

A

Triglycerides and cholesterol

They have to be transported as lipoproteins

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3
Q

What is located on the outer coat of lipoproteins?

A

Phospholipids
Free cholesterol
Proteins (apoproteins)

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4
Q

What is located on the inner coat of lipoproteins?

A

cholesterol
cholesterol esters,
Triglycerides
Vitamins (e.g. A and E)

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5
Q

What are the three main transportation paths for lipoproteins?

A

Gut (food)—–> rest of the body
Liver——–> Peripheral tissues
Peripheral tissues——-> liver

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6
Q

What do apoproteins determine in the lipoprotein?

A
  • Fate of the lipoprotein
  • Interactiosn of the lipoprotein
  • Inhibition and activation of certain enzymes
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7
Q

How are reactive oxygen species formed in the TCA cycle?

A

When electrons are not transported efficiently

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8
Q

What are reactive oxygen species?

A

High energy molecules

Cause damage of proteins, lipids, DNA

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9
Q

What is hypoxia? What is its effect on ROS’s

A

Low oxygen concentration

Causes the production of more ROS’s as there is a low amount of oxygen to mop up electrons

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10
Q

How do cells adapt to hypoxic situations?

A

Limits the amount of ATP needed
Improves the efficiency of anaerobic ATP production
Limits oxidative stress to prevent tissue damage

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11
Q

Which gene/protein enables the tissue to adapt to hypoxic situations? How does it work?

A

Hypoxia-induced factor-1 (HIF1)
During normal conditions HIF1 is broken down
During hypoxia, HIF1 is activated and moves to the nucleus where it acts as a transcription factor switching on genes which enable the cell to survive low oxygen conditions

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12
Q

What does activation of HIF1 cause?

A

Reduces mitochondria by promoting its degradation
Inhibits synthesis of new mitochondria by blacking PGC1 activity.
So less TCA less ROS produced

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13
Q

How is HIF1 an oncogen?

A

Allows cancer less to survive in low oxygen environments. Potential target for cancer drug therapy

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14
Q

What is leigh syndrom? What does it cause?

A

Genetic hereditary mutation in the genes for ECT causing loss of oxidative metabolism in ATP production.

Causes death to cells dependant on ATP e.g brain, nerves muscles
Death after 2/3 years (respiratory)

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15
Q

What is the main component and apoprotein in

Chylomicrons, VLDL,IDL,LDL and HDL?

A 
Chylomicrons- Comp-TAG apo-B48
VLDL- comp-TAG apo-B100(A,C,E)
IDL- comp- TAG, cholestral apo-B100(E)
LDL-comp- cholestral apo- B100
HDL- comp-protein apo-AI,AII
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16
Q

What is the function of apoB-100?

A

Controls the metabolism of LDL’S

17
Q

What is the function of B48?

A

Controls the uptake of chylomicrons

18
Q

What is the function of ApoE and Apo C

A

Apo E- controls the binding of lipoproteins to receptors on the cell membrane
Apo C- Enzyme inhibitor

19
Q

What is the function of Chylomicrons? How is it formed?

A

Formed in the gut- during digestion

Carries fat/ cholesterol from GI to peripheral tissues

20
Q

What is the function of VLDL? How is it formed?

A

Formed in the liver

carries triglycerides to peripheral tissues

21
Q

How is it IDL formed?

A

Formed from partly absorbed VLDL in periphery

22
Q

How is it LDL formed?

A

remnants of VLDL and IDL which enter circulation and transport cholesterol around to peripheral tissues

23
Q

What are HDL’s?

A

Scavengers of cholesterol from peripheral tissue which transport cholesterol esters to the liver to make VLDL and LDL

24
Q

Describe the metabolism of chylomicrons

A

Absorbed from fats and cholesterol, absorbed from the GI and pass into the lymphatics before entering the blood
In lymphatics they interact with HDL which donates Apo E and C2

25
Q

Functions of Apo E and C2 in relation to chylomicrons

A

ApoE- Allows chylomicron remnants to be taken up by the liver
ApoC2- Allows chylomicrons to give TAG to peripheral tissues

26
Q

Describe the formation of VLDL

A

Produced by the liver
Requires the addition of ApoC2 and ApoE from HDL to mature
Remanats are either reabsorbed by the liver or become LDL

27
Q

What is the function of lipoprotein lipase?

A

Breaks down TAG in chylomicrons and VLDL’s into free fatty acids which can be taken up by periphery cells

28
Q

Which apoprotein acn activate lipoprotein lipase?

A

ApoC2

29
Q

Describe lipoprotein lipase activity during starvation

A

Activity is highest in muscles where FA are used to make ATP from the TCA cycle

30
Q

During starvation what happens to fat?

A

Its is transported from liver to muscle to be used to make energy

31
Q

Describe lipoprotein lipase activity after a meal

A

Activity is highest in adipose to form fat via esterficaction

32
Q

What do chylomicrons and VLDL’s mostly transport?

A

TAG

33
Q

Which lipoprotein mostly transports cholestral?

A

LDL’s

34
Q

How are IDL’s converted into LDL’s?

A

IDL’s are absorbed by the liver

The enzyme hepatic TAG ligase converts IDL’s to LDL’s (high in choesteral, only has Apo100)

35
Q

How is LDL taken up by target cells?

A

ApoB100 binds to LDL receptors on target cells and allows receptor mediated endocytosis (taken up by target cells)

36
Q

Why can LDL’s stay longer in circulation?

A

They lack ApoE

37
Q

What is familial hypercholesterolemia?

A

Autosomal dominant genetic condition
Causes mutations in 3 genes:
1. LDLR- receptor for receptor mediated endocytosis of LDL’s
2. PSCK9- Kinase enzyme which controls the amount of LDL receptor produced
3. APOB- Gene for ApoB 100 which binds to LDL receptor on target cells

Causes high levels of LDL to accumulate in the blood

38
Q

List the important functions of HDL

A

Can exchange molecules (apoproteins,cholesterol,TAG) with other lipoproteins
Made in the liver and small intestine
Transports used cholesterol back to the liver for disposal
When produced in the liver it makes mainly ApoA1

Biochemistry (7 decks)

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