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CVR > Blood Lipids and Lipoproteins > Flashcards

Blood Lipids and Lipoproteins Flashcards

1
Q

What is the structure of cholesterol?

A

4-ring structure with 27 carbons

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2
Q

What are the sources of cholesterol?

A
  1. Exogenous (diet)- 1g/day

2. Endogenous (synthesised in liver, intestines, adrenal glands and reproductive tissues)- 0.5-1g/day

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3
Q

What are the steps in the synthesis of Cholesterol?

A
  1. Synthesis of Isopentenyl Pyrophosphate
  2. Formation of Squalene from 6 Isopentenyl Pyrophosphate
  3. Cyclisation of Squalene to form Cholesterol
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4
Q

What happens during the synthesis of Isopentenyl Pyrophosphate?

A
  1. Acetoacyl CoA + Acetyl CoA–> HMG-CoA
  2. HMG CoA–> Mevalonate
  3. Mevalonate–>–>–>–> Isopentenyl Pyrophosphate
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5
Q

How is HMG-CoA converted to Mevalonate?

A

It is reduced by HMG-CoA Reductase

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6
Q

How is Mevalonate converted to Isopentenyl Pyrophosphate?

A

It undergoes phosphorylation reaction:

1. Mevalonate–> 5-Phospho Mevalonate–> 5-Pyrophospho Mevavlnate–> Isopentenyl Pyrophosphate

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7
Q

What happens in the formation of Squalene from 6 Ispoentenyl Pyrophosphate?

A

The 6 Isopentenyl Pyrophosphate molecules are joined together via condensation reactions

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8
Q

What happens in the cyclisation of Squalene to form cholesterol?

A
  1. Squalene is oxidised to Squalene 2,3-Epoxide
  2. Squalene 2,3-epoxide is cyclised to Lanosterol
  3. Lanosterol loses 3 Methyl Groups and 1 double bond, and 1 double bond is shifted to make cholesterol
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9
Q

How is the synthesis of Cholesterol regulated in the body?

A

Controlled by negative feedback mechanism mediated primarily by changes in the amount/activity of HMG-CoA Reductase

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10
Q

How is the amount/activity of HMG-CoA Reductase controlled in the body?

A
  1. Control of the Rate of Synthesis of Reductase mRNA
  2. Control of the Rate of translation of reductase mRNA
  3. Degradation of the Reductase
  4. Phosphorylation of the Reductase
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11
Q

How is the rate of synthesis of HMG CoA reductase mRNA controlled?

A

When Cholesterol levels are low, Sterol Regulatory Element Binding Protein (SREBP) binds to the Endoplasmic Reticulum and promotes transcription of HMG-CoA Reductase mRNA

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12
Q

How is the rate of translation of HMG CoA reductase mRNA controlled?

A

It is inhibited by non-sterol metabolites derived from mevalonate and dietary cholesterol–> Negative feedback from production of cholesterol

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13
Q

When does degradation of the HMG CoA Reductase occur?

A

When there is too much cholesterol, the enzyme can mark itself for ubiquitination/proteolysis (suicide)

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14
Q

What does phosphorylation do to HMG CoA Reductase?

A

Decrease the activity of the reductase in response to low levels of ATP

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15
Q

How is cholesterol transported in the body?

A

Transported in the form of lipoproteins–> VLDL, LDL, HFL

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16
Q

How is Cholesterol Pharmacologically regulated?

A
  1. Statins inhibit HMG-CoA Reductase
  2. Sequestering Bile Acids in the Intestine–> Cholestramine and Coletipol reduce absorbance of exogenous cholesterol
  3. Altering the relative levels of different lipoproteins–> Decrease amounts of VLDL and LDL
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17
Q

What are the derivatives of Cholesterol?

A
  1. Bile Salts
  2. Steroid Hormones
  3. Vitamin D
18
Q

What is the function of Bile Acids and Bile Salts?

A

Elimination of Cholesterol from the body by conversion of Cholesterol into Bile Acids and Bile Salts which can be excreted

19
Q

How are Bile Acids and Bile Salts made from Cholesterol?

A

Cholesterol is hydroxylised by 7a-hydroxylase to from 7a-hydroxycholesterols Cholic acid or Chenodeoxycholic Acid (Bile Acids). Bile Acids are combined with either Glycine or Taurine in the Liver to form Bile SaltsE.g. Glycocholic Acid

20
Q

What happens when Bile Salts are exposed to bacterial flora of the intestine?

A
  1. Generation of bile acids by removal of the glycine or taurine
  2. Production of secondary bile salts by the removal of an -OH group
21
Q

Where are Bile Salts Synthesised?

A

Liver

22
Q

Where are Bile Salts stored?

A

Gall Bladder

23
Q

Where are Bile Salts released?

A

Small Intestine

24
Q

What is Cholesterol Gall-Stone Disease?

A

There is not enough bile salts being secreted to handle the amount of cholesterol being secreted–> so the cholesterol precipitates in the gall bladder

25
Q

What Steroid Hormones are derived from Cholesterol?

A
  1. Progesterone (prepares lining of uterus for implantation of ovum)
  2. Androgens (Development of male secondary sex characteristics)
  3. Estrogen (Development of Female Secondary Sex Characteristics)
  4. Glucocorticoids (Promotes Gluconeogenesis and inhibits inflammatory response)
  5. Mineralocorticoids (Act on distal tubule of kidney to reabsorb NA+ and excrete K+ and H+
26
Q

How is Vitamin D formed from Cholesterol?

A

7-dehydrocholesterol is photolysed by UV light to pre-Vitamin D3, which isomerise to Vitamin D3–> converted to Calcitriol in the liver and kidneys

27
Q

What are the Lipoproteins?

A
  1. Chylomicrons
  2. HDL
  3. LDL
  4. VLDL
28
Q

What are the functions of Lipoproteins?

A
  1. Transport of lipids to and from tissues

2. Keep their lipid components soluble for transport in plasma

29
Q

What are the functions of Apolipoproteins?

A
  1. Essential structural components
  2. Non-essential structural components
  3. Ligands for cell-surface receptors
  4. Coenzymes for lipid metabolism enzymes
30
Q

What are the steps of Chylomicron Metabolism?

A
  1. Apolipoprotein synthesis (B-48 in rough ER)
  2. Lipid Synthesis (in Smooth ER)
  3. Chylomicron Assembly (in Golgi)
  4. Maturation (in blood plasma, receive Apo C and Apo E)
  5. Utilisation of chylomicron triglycerides by tissues (LPL activated by Apo C-II to degrade triglycerides in chylomicron to release Fatty Acids and Glycerol)
  6. Clearance of Chylomicron Residues–> Liver takes back “empty” chylomicrons (recognise Apo E)
31
Q

What does VLDL transport in the body?

A

Endogenously synthesised Triglycrerides

32
Q

What does LDL transport in the body?

A

Endogenously synthesised Cholesterol from liver to tissues

33
Q

What does HDL Transport?

A

Cholesterol from tissues back to liver

34
Q

What happens in VLDL Metabolism?

A

Same as Chylomicron Metabolism but with Apo B-100 instead of Apo B-48

35
Q

How does VLDL become LDL?

A
  1. Losing Apo E and Apo C back to HDL

2. Exchanging lipids with HDL (give away triglycerides and phospholipids in exchange for cholesterol)

36
Q

What is special about LDL receptors on tissues?

A

They recognise Apo B-100 (not Apo B-48) and Apo E

37
Q

What happens in LDL Metabolism?

A

LDL (mostly Oxidised-LDL) are taken up by Macrophages which express high levels of Scavenger Receptor Class A–> transform into “Foam Cells”–> Form Atherosclerotic Plaques

38
Q

What happens in HDL Metabolism?

A

Nascent HDL containing Apo A,C and E accumulate cholesterol

39
Q

What are the functions of HDL?

A
  1. Reservoir of apolipoproteins (Apo-CII and ApoE)
  2. Accumulate unesterified cholesterol
  3. Rapid Esterification of Cholesterol
  4. Reverse cholesterol transport
40
Q

What is Hypertriglyceridaemia?

A

Disorder of VLDL and Chylomicrons–> too much VLDL and Chylomicrons in the blood

41
Q

What is Hypercholesterolaemia?

A

Disorder of LDL–> too much cholesterol/LDL in the blood

42
Q

What is Tangier Disease?

A

Disorder of HDL–> Low Plasma HDL cholesterol

CVR (5 decks)

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