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Lipids And Lipoproteins Flashcards

1
Q

What is the building block for synthesis of all isoprenoids?

A

IPP - Isopentenyl pryophosphate

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2
Q

What makes IPP? How many carbons will it have?

A

3 Acetyl CoAs (2 C compounds) —> IPP (5C compound)

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3
Q

What will isoprenoids include?

A
  1. Steroid
  2. Lipid soluble vitamins
  3. Others (ubiquinone, dolichol, lipid anchors)
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4
Q

What are some examples of steroids?

A

Cholesterols

Bile acids

Steroid hormones

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5
Q

What are the lipid soluble vitamins?

A

K
A
D
E

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6
Q

Where can Acetyl CoA come from (3) ?

A

In mitochondria from

  1. Oxidative decarboxy of pyruvate
  2. Beta ox of FAs
  3. Breakdown of AAs
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7
Q

How is Acetyl CoA transported into the cytoplasm?

A

Via citrate shuffle

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8
Q

What is the tetracycline sterane ring made form?

What is this the backbone of?

A

Six units of IPP

Backbone of most steroids

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9
Q

What is the structure of cholesterol?

How many carbons does it have?

A

Allicyclic compound made of 4 fused rings of sterane

27 carbons

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10
Q

What is the allocation of carbons in cholesterol?

A

Sterane = 17 Cs
Side chain = 8 member hydrocarbons

2 methyl groups

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11
Q

Where is the double bond in cholesterol?

Hydroxyl group?

A

One double bond b/w C5 and C6

Hydroxyl group at C3

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12
Q

What is the most abundant sterol?

A

Cholesterol

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13
Q

Why is cholesterol so important?

A

Component of PMs & precursor of biologically active compounds such as
‣ 1. Bile acids and bile salts
‣ 2. Vit. D
‣ 3. Steroid hormones

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14
Q

What are examples of steroid hormones?

A 
Progesterone
Aldosterone
Cortisol
Testosterone
Estradiol
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15
Q

What happens to the steroid nucleus of cholesterol?

A

Can NOT be degraded

Has to be used biochemically or excreted

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16
Q

What happens if there is an excess of cholesterol?

A

Atherosclerosis

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17
Q

What is the relationship b/w biosynthesis of cholesterol and dietary intake?

A

Inversely proportional

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18
Q

What is the overall formula for the synthesis of cholesterol?

A

18 Acetyl CoA + 18 atp + 16 NADPH + 16 H + 4 O2

=
Cholesterol + 16 nadp + 18 ADP + 18 Pi

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19
Q

What are the 2 phases of cholesterol synthesis?

A

Phase 1: generation of IPP from Acetyl CoA

Phase 2: generation of cholesterol from IPP

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20
Q

What is the rate limiting enzyme of cholesterol synthesis?

A

HMG CoA Reductase

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21
Q

What is the target of statins in order to lower cholesterol?

A

HMG CoA Reductase

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22
Q

Where is HMG CoA reductase located and what is its strucutre?

A

8 pass transmembrane ER protein w/ catalytic domain in Cytosol

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23
Q

How do Statins work? In order to do what?

A

Strong competitive inhibitor of HMG CoA reductase with an extremely high affinity

-leads to reduced cholesterol levels

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24
Q

What is hypocholesterolemic action due to via Statins?

A

Due to increase in Sterol Reg. Element binding Proetin maturation

Increase in SREBP —> transcription of LDL R. —> enhanced clearance of cholesterol via LDL mediated endocytosis

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25
Q

What are the side effects assoc. w/ Statins?

A

Mediate myopathy due to depletion of msucle levels of ubiquinone (CoQ 10) - leading to impairment of mitochondrial funciton

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26
Q

If you have a pt. On statins - what must you supplement them w/?

A

W/ CoQ 10

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27
Q

What happens to cholesterol after it is synthesized?

A

Esterified to cholesterol esters by ACAT

Packaged into VLDL and released into blood

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28
Q

What is the full pathway of cholesterol synthesis?

A 
Acetyl CoA + Acetyl CoA 
—> acetoacetyl coA + Acetyl CoA (HMG CoA synthase) 
—> HMG CoA (HMG CoA Reductase) 
—> mevalonate
—> IPP
—> 6 IPP 
—> squareness
—> lanosterol
—> cholesterol
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29
Q

What provides positive feedback to HMG CoA Reductase?

A

Insulin, thyroxine

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30
Q

What provides negative feedback to HMG CoA reductase ?

A 
Glucagon
Sterols
High AMP 
Vit. E 
Statins
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31
Q

What will inhibit formation of cholesterol from lanosterol?

A 
Anoles
KCN
Tamoxifen
Morpholine 
Triparanol
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32
Q

What directly inhibits HMG CoA Reductase?

A

FFAs
Bile acids
Oxysterols
Statins

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33
Q

What covalent modification will

Inactivate HMG CoA reductase? Done by what?

Activate? Done by what?

A
  • phospho form = inactive
  • during conditions of low energy
  • done by glucagon
  • dephospho form = active
  • done by insulin
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34
Q

What is the transcriptional control of HMG CoA reductase?

A

HMG gene’s Sterol REgulatory element in promoter region

SRE-biding proteins —> SRE
SREBP + SCAP (SREBP cleavage activating protein)
SREBP -SCAP + INSIG

Low cholesterol = translocation of SREBP-SCAP to Golgi

Cleaved to release mature SREBP (will dimerize)

SREBP —> SRE at nucleus —> promotes transcription of. HMG CoA reductase

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35
Q

What does the binding of SREBP at the SRE promoter region of the HMG gene do?

A

Unregulated enzymes in cholesterol biosynthesis pathway

Increase transcription of HMG CoA reductase

Unregulated LDL R.

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36
Q

What is translational control of cholesterol synthesis?

A

At protein synthesis level

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37
Q

What is the post-translation control of cholesterol synthesis?

A

At level of protein turnover/degradation

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38
Q

What is the function of Lipoproteins?

A

Serve as vehicles of transport for

  • cholesterol
  • cholesterol esters
  • TAGs
  • fat soluble vitamins
39
Q

What is the structure of Lipoproteins?

A
  1. Outer shell
    - mono layer of phospholipids, free cholesterol, and apolipoproteins
  2. Inner shell (hydrophobic)
    - packed w/ TAGs, choelsterol, Cholesterol esters
40
Q

How do Lipoproteins contribute to lipid metabolism?

A

‣ Will transport and deliver tags
‣ Have role in cholesterol homeostasis
• Transports it from sites of synthesis—> use & to liver for excretion

41
Q

What are Apolipoproteins?

A

Targeting signals/ligands for Receptors to internalize lipoproteins

-activate various enzymes involved in lipoprotein metabolism and processing

42
Q

What are the 5 major types of lipoproteins?

A
  1. Chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
43
Q

What are the characteristics of Chylomicrons?

A

◦ Most TAGs, Least Protein
◦ Exogenous, formed from dietary fats
◦ Largest
◦ Least dense

44
Q

What are the enzymes found on chylomicrons?

Function?

A

‣ 1. ApoB-48
• Facilitates transport

‣ 2. ApoC-II
• Activates capillary lipoprotein lipase

‣ 3. ApoE
• Facilitates uptake into liver

45
Q

What are the characteristics of VLDL?

A

Made in liver

Packaged w/ TAGs and choelsterol

46
Q

What are the enzymes on VLDL?

A

ApoB-100

ApoC-II

ApoE

47
Q

What are the characteristics of IDL?

A

Made from VLDL

-no ApoCII

(Just apoE and apoB-100)

48
Q

What are the characteristics of LDL?

A

Made from IDL

Bad choelsterol

Uptakes into cells

No ApoE or ApoC-II (just ApoB-100)

49
Q

What are the characteristics of HDL?

A

Good cholesterol”
◦ Smalles
◦ Most dense
◦ High protein and phospholipid content

50
Q

What enzymes are found on HDL?

A

‣ ApoA-1
• Activates enzyme that esterifies cholesterol

‣ ApoE
• Promotes uptake into hepatocytes (different than apoE in chylomicrons)

‣ ApoC-II
• Activates capillary lipoprotein lipase

51
Q

How are chylomicrons processed?

A
  1. Baby chylomicrons assembled w/ dietary lipids in Sm. Int.
    - transported thru lymphatics to blood
    - only has ApoB-48
  2. ApoC-II and ApoE supplied by HDL —> mature chylomicrons
  3. Cap. Lipoprotein Lipase hydrolyzes TAGs —> glycerol & FFAs
    - apoC II released back to HDL
  4. Remnants bind via ApoE to liver and are endocytosed

—> VLDL

52
Q

How is VLDL made into IDL and LDL?

A
  1. VLDL in liver —> blood
  2. Cap. Lipoprotein lipase + tags —> glycerol and FFAs
    - apoCII back to HDL
    - now is IDL
  3. IDL cholesterol —> liver via binding of apoE
    - loses Tags and apoE
  4. LDL formed —> delivers chol. To liver and peripheral tissues via ApoB-100 binding
53
Q

How does aterhosclerosis occur?

A

Due to accumulation of LDL

54
Q

What is the major carrier of cholesterol in the blood?

A

LDL

55
Q

How is the LDL particle strucutres?

A

Shell of phospholipids and free cholesterol

Packed w/ 1500 cholesterol ester molecules in core

56
Q

What is the role of LDL?

A

‣ Transport cholesterol to peripheral tissues and regulate de novo synthesis of cholesterol at these sites

57
Q

How is LDL uptaken?

A

Via R. Mediated endocytosis

-becomes engulfed in clathrin coated vesicles
—> endosome
—> lysosome
—> free cholesterol

58
Q

What is Familial HYPERchoelsterolemia

A

Mutations that generate receptors unable to release LDL cargo

59
Q

How is HDL processed?

A
  1. Disc-shaped baby lipid poor HDL = synthesized in liver and Small intestine
  2. Baby HDL + cholesterol from peripheral tissues
  3. LCAT esterifies cholesterol
    ‣ Via transfer of FA
    ‣ Cholesterol esters enter HDL core —> make it spherical = mature
60
Q

How do HDL and chylomicrons interact?

A

HDL donates and receives APoC-II and ApoE from chylomicrons

61
Q

How does HDL interact w/ VLDLs, IDLs, and LDLs?

Facilitated by?

A

Transfer chol. Esters to them in exchange for TAGs and phospholipids

Facilitated by CETP (chol.ester transfer protein)

62
Q

Where will HDL deliver cholesterol to?

A

To liver

VLDL, IDL, and LDL also to liver

63
Q

What is HDL crucial for?

A

for maturation of chylomicrons

• Via supplying ApoC-II and ApoE

64
Q

What reduced risk is assoc. w/ high HDL?

A

Reduced risk for Coronary A. Disease

65
Q

What chol. Transport is HDL involved in?

Why?

A

Reverse chol. Transport

Bc it removes LDL from periphery and transport it to liver where it can be recycled and processed

66
Q

How does HDL facilitate LDL transport?

A

ApoA-1 of HDL —> ABCA1

ABCA1 = atp binding cassette transporter

67
Q

What disease is caused from the loss of ABCA1?

Characterized by?

A

Tangier disease

Charac. By HDL deficiency, chol. Accumulation in macrophages, premature atherosclerosis

68
Q

What do foam cells facilitate?

A

Facilitate formation of plaques

69
Q

What properties does HDL possess?

A

Antioxidant, anti-inflamm., antithrombotic, and NO-inducing properties

Inhibits oxidation of LDL

Keeps inner wall of blood vessels (endoth.) healthy

70
Q

What can increase HDL-C levels?

A

Weight loss, exercise and smoking cessation

-antihyperchol. Drugs, vibrates, anti-diabetic thizolindine drugs, estrogens, and omega 3 FAs

71
Q

What is the overall integration of lipoprotein synthesis?

A

◦ Chylomicron matures in Sm. Int.
‣ Receives ApoC-II and ApoE from HDL
◦ Capillary lipoprotein lipase will remove FFAs from it
‣ APoC-II is released back to HDL
◦ Chylomicron remnant —> liver
◦ VLDL assembled in liver and released to blood
‣ Exchanges TAGs and phospholipids w/ HDL via CETP
‣ Receives APo-CII and ApoE from HDL
◦ capillary lipoprotein lipase will remove FFAs from VLDL
‣ ApoC-II back to HDL
◦ IDL formed
‣ Exchanges TAGs and phospholipids w/ HDL via CETP
◦ capillary lipoprotein lipase will remove FFAs from VLDL
‣ ApoE is lost
◦ LDL’s ApoB-100 binds to LDL Rs. On peripheral tissues
◦ Drops off cholesterol to tissues
◦ Baby HDL will come and pick up cholesterol
◦ Baby HDL —> LCAT —> mature HDL

72
Q

What is Type 1 HYPER-lipoproteinemia due to?

A

Deficiency in apoC-ii or defective lipoprotein lipase

73
Q

What are the effects of Type I Hyper-lipoproteinemia?

A

Increased chylomicrons

Increased TAGs

74
Q

What is Type II HYPER-lipoproteinemia due to?

Effects?

A

Complete or partially defective LDL r.
Impaired ability to recognize ApoB-100 on LDL by liver/peripheral tissues

-increased chol, tags, ldls, VLDL

75
Q

What is type 1 hyper-lipoproteinemia also called?

A

Hyper-chylomicrons is

76
Q

What will the deficiency in cap lipoprotein lipase/apoC-II seen in type 1 hyperlipoproteinemia cause?

A

Causes

  1. Inability to hydrolyze TAGS in chylomicrons and VLDL
    - plasma TAG levels > 1000 mg/dL
77
Q

What are the Sxs of Hyper-lipoproteinemia?

A

•!!!!! Creamy appearance of blood sample

• Abdominal pain
• Acute pancreatitis
• Cutaneous eruptive xanthomas
◦ Nodules of cholesterol in skin and tendons

78
Q

What is the inheritance pattern of Type 1 hyper-lipoproteinemia?

A

Autosomal recessive

79
Q

Tx. For type 1 hyper-lipoproteinemia?

A

Low fat diet

Bc it has increased. Chylomicrons which are made by dietary fat

80
Q

What does the Defective LDL R. In Type II Hyper-lipoproteinemia cause?

A

Causes

  1. Increased cholesterol in blood
  2. Oxidation of xs LDL —> lead to devel. Of CV diseases like atherosclerosis
81
Q

What is the inheritance pattern of Type II hyper-lipoproteinemia?

A

Autosomal dominant

82
Q

What is Type II Hyperlipoproteinemia also known as?

A

Hyper-cholesterolemia

83
Q

What is the normal level of chol?

If you are heterozygous for TYpe 2 hyperlipoproteinemia?

If you are homozygous?

A

Normal: 130-200

Heterozygous: 300-500

Homozygous: >800 (left untreated - will indie of CAD before teenage yrs.)

84
Q

What are the Sxs of Type 2 hyperlipoproteinemia?

A

Xanthomas
Corneal deposits in eyes
Angina pectoral

85
Q

What is the tx for

Homozygous type 2 hyperlipoproteinemia pts.?

Heterozygous pts?

A

Homo: need LDL apheresis; liver transplant

Hetero: respond to diet, statins, bile acid binding resins

86
Q

What is HYPO-lipoproteinemia due to?

Effects?

A

Due to defect in transporter that supports chol. Pickup by baby HDLs

-decreased HDL (bc can’t mature)

87
Q

What happen when LDL-C accumulates under endothelial cells lining blood vessels?

A

Combine with reactive oxygen species and form Oxidized LDL (oxLDL)

88
Q

Where will oxLDL accumulate?

A

In vessel wall

89
Q

What will accumulation of oxLDL in vessel wall lead to?

A

Endothelial injury and dysfunction

Promoting further influx of LDL bc of increased vasc. Permeability and leukocyte adhesion

90
Q

What is initiated due to oxLDL?

A

Inflammatory response where macrophages take up oxLDL

91
Q

What will macrophages form with oxLDL?

A

Foam cells

92
Q

What do trapped foam cell form?

A

Plaques

93
Q

How does arterial plaque develop?

What does this lead to?

A

Thru the death of foam cells, platelet adhesion, and recruitment of sm. M. Cells

Eventually leads to atherosclerosis

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