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Nutrition and Metabolism > Lipid synthesis and transport in the blood > Flashcards

Lipid synthesis and transport in the blood Flashcards

1
Q

Definition of plaque

A

Complex structure involving inflammation and proliferation of smooth muscle in artery wall. Contains connective tissue and pool of cholesterol

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2
Q

Definition of foam cells

A

Macrophages filled with lipid, mainly cholesterol

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3
Q

Describe the use of lipids as a store of fuel

How is excess carbohydrate stored in the long term

A

Energy providing food consumed in quantities greater than needed at the time
Fuel stored
Carbohydrate stored as glycogen, limited store
Long term reserve is lipid as TAGs

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4
Q

What happens when glycogen storage is full

A

Glucose converted to TAGs in the adipose tissue

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5
Q

How are fatty acids synthesized
Formation of malonyl CoA from Acetyl CoA
What does malonyl CoA inhibit

A

Enzyme stimulated by insulin in fed state in the cytosol

Normally, acetyl CoA not found in the cytosol.

  • Acetyl CoA + Oxaloacetate =(citrate synthase)=> Citrate =(moves into cytosol=>
  • Citrate =(ATP citrate lyase)=> Acetyl CoA + Oxaloacetate

-Acetyl CoA + ATP + CO2 =(Acetyl CoA carboxylase)=> Malonyl CoA + ADP + Pi (rate limiting step)

Malonyl CoA signifies fed state
Malonyl CoA inhibits carnitine transferase

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6
Q

How are fatty acids synthesized

Elongation of carbon chain

A

Acetyl CoA + CO2 =(fatty acid synthase + NADPH)=> Malonyl CoA

Malonyl CoA + Acetyl CoA =(fatty acid synthase + NADPH)=> 4 carbon chain + CO2

4 carbon chain + Malonyl CoA =(fatty acid synthase + NADPH)=> 6 carbon chain + CO2

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7
Q

Why is fatty acid synthase special

A

Made up of many enzymes and a large AS

Hydrogenate then dehydrate

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8
Q

How is TAG synthesised
What is it synthesised from in glycolysis

How are TAGs then processed to form lipoproteins

A

In the liver

  • Dihydroxyacetone phosphate => glycerol phosphate
  • Glycerol phosphate + 3 FA => TAG + Pi

TAG + other lipids + apoproteins = TAG,Apoprotein,Phospholipid,Cholesterol

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9
Q

Why are apoproteins bound to TAG

A

Apoproteins don’t function on their own

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10
Q

Describe the structure of a lipoprotein
What 2 structures are found in the inner core
What 3 structures are found in the membrane

A

Inner core
-TAGS
-Cholesterol esters (can’t form membranes)

Outer shell

  • Single phospholipid layer
  • Cholesterol (unesterified)
  • Apoproteins (hold structure together, activate enzymes, recognition of other cells)
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11
Q

2 main properties of lipoproteins

A

Lipids insoluble in water

Needs to be transported as a lipid protein complex

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12
Q

3 main properties of apoproteins

A

Structural role
Recognized by receptors
Activate certain enzymes in lipid metabolism

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13
Q

4 classes of lipoproteins and their properties

A

Chylomicrons
-Largest, lowest density, carry mainly dietary TAG

Very low density lipoprotein (VLDL)
-Carries mainly endogenous TAG

Low density lipoprotein (LDL)
-Carries mainly cholesterol to the tissues

High density lipoprotein (HDL)
-Carries mainly cholesterol from tissues to the liver

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14
Q

Transport of exogenous fat

A 
Nascent chylomicron (TAG, CE, C, apoB48)  from small intestine
Nascent chylomicron joins to apoC2, apoE (from HDL) to form a chylomicron
Lipoprotein lipase (LPL, insulin activated) in the capillary endothelium hydrolyses the chylomicron into FFA, glycerol, (TAG, CE, C, apoB48, apo E as 1 unit) 
ApoC2 returns to HDL

FFA rebuilt up to form TAG in adipose

TAG, CE, C, apoB48, apo E, (remnant chylomicron) binds to apoE receptor on liver where it is broken down

Glycerol also enters the liver

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15
Q

Transport of endogenous fat

A

TAG, CE, C, apoB100 (VLDL) unit leaves liver and binds with apoC2, apoE (VLDL)

VLDL transported in the capillaries to LPL where it is broken down into FFA into the tissue, glycerol to the liver and the remainder forms IDL

IDL (CE, C, TAG, apoC, apoE, apoB100) splits so apoB100 and CE, C, TAG form LDL. Remaining apoE and apoC2 returned to HDL

. 50% of these LDLs enters peripheral tissue via B receptors, the other 50% enters the liver and is broken down

ApoC, ApoE returns to HDL which can be transferred to VLDLs

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16
Q

Role of HDL in lipid transport

A

HDL generated by liver and small intestine as cholesterol free lipoproteins and apoA1.

LCAT (lecithin cholesterol acyl transferase), activated by apoA1, takes C from peripheral tissues and converts it into CE by adding 1 FA from PC. CE is sequestered into HDL core. PC becomes LPC

When HDL is full, inhibits LCAT. CETP used to transfer some CE to VLDLs so HDL can continue to remove C from cells
SR-B1, HDL receptor so cholesterol esters can be used in the liver

17
Q

Describe the receptor mediated endocytosis of LDL

A

LDL binds to receptors on cell surface and are taken up by endocytosis.

The receptors are recycled and are ready to receive more LDL from the cell surface

Lysosomes of LDL are formed

Enzymes of cholesterol synthesis (HMG CoA) lead to cholesterol synthesis from LDL

Cholesterol controls its own synthesis and the no of LDL receptors on the cell surface by controlling the amount of translation for the receptors

18
Q

How is cholesterol synthesised

A

Acetyl CoA + Acetoacetyl CoA
HMG CoA =(HMG CoA reductase)=> Mevalonate
Cholesterol

19
Q

How is cholesterol synthesis controlled

A

If we consume cholesterol, cholesterol synthesis is inhibited

20
Q

LDL receptors and the effects of LDL receptor deficiency

A

Recognize B100
Remove LDL from the circulation
Receptor mediated =endocytosis

Deficiency of LDL receptors (familial hypercholesterolemia)
V high blood cholesterol levels
Premature death from atherosclerosis

21
Q

Hyperlipidaemias

What are the 2 types

A

Hypercholesterolemia
Hypertriglyceridaemia

Has a genetic/environmental element

22
Q

What are the 4 types of genetic hyperlipoproteinaemias

A

Defective LDL receptor
Lipoprotein lipase deficiency
Deficiency of apoC2
Deficiency of apoproteins involved in remnant uptake

23
Q

What can happen if there is a defective LDL receptor

A

Hypercholesteralaemia

Increases LDL in blood

24
Q

What can happen if there’s a lipoprotein lipase deficiency / apoC2 deficiency

A

Increase chylomicrons and VLDL

25
Q

What can happen if there’s a deficiency of apoproteins involved in remnant uptake

A

Increase in chylomicrons and VLDL remnants

26
Q

Risk factors for secondary hyperlipoproteinaemias

A 
Obesity
Diabetes mellitus T2
Dietary FA SFA vs PUFA
  omega 6 PUFA, lower cholesterol
  omega 3 lower TAG
Alcohol
27
Q

Lipoprotein a
What is it
What pathologies is it associated with

A

In high conc associated with increased CHD risk
LDL + apoa
Levels are genetic, can be increased by trans fat, decreased by estrogen
Slows breakdown of blood clot by competing with plasminogen

28
Q

Relationship between average serum cholesterol and mortality for CHD

A

Increased serum cholesterol, increased mortality for CHD

29
Q

Relationship between average HDL cholesterol and mortality for CHD

A

Increased HDL cholesterol,

Decreased mortality for CHD

30
Q

Describe atherosclerosis

A

Complex structure involving inflammation and proliferation of smooth muscle in artery wall
Contains connective tissue and a pool of cholesterol rich lipid
Starts as fatty streak from accumulation of foam cells
Foam cells absorb LDL

Foam cells=macrophages, lipid filled, mainly cholesterol

31
Q

Describe normal LDL metabolism

A

Cholesterol synthesis in the liver

Cholesterol released into the blood as VLDL
LPL results in FFA absorption into peripheral tissues, glycerol to liver and remnants as IDL

HL (hepatic lipase) hydrolyses TAGs in IDL to form LDL

50% of LDL goes to extra hepatic cells via B receptors
50% of LDL goes to the liver to be broken down again

No LDL enters the macrophages

32
Q

What happens when the LDL is modified and oxidized?

A

Not recognized by normal B100 receptors, taken up by scavenger receptors in foam cells
Receptors not down regulated, results in accumulation of cholesterol in foam cells

Instead of LDL entering the liver for breakdown, it all enters the macrophages

Nutrition and Metabolism (14 decks)

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