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BPK 458 > Module 4: Biochemistry, Lipid Metabolism and Lipid Pathology > Flashcards

Module 4: Biochemistry, Lipid Metabolism and Lipid Pathology Flashcards

1
Q

Review relevant lipids of physiologic significance.

A

a

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2
Q

List the major classes of lipoproteins and describe their lipid and apoprotein composition.

A

a

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3
Q

Discuss lipid metabolism.

A

a

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4
Q

List the four lines of evidence linking cholesterol to atherosclerosis.

A

a

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5
Q

Differentiate between different forms of dyslipidemias.

A

a

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6
Q

What are the 2 classifications of lipids

A

Simple and Complex

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7
Q

What are simple lipids. Give examples

A
  • Simple: a FATTY ACID ESTER of DIFF ALCOHOLS and carries NO OTHER SUBSTANCE; such as fats and waxes.
  • > Fats: Esters of fatty acids with GLYCEROL.
  • > Waxes: Esters of fatty acids with higher molecular weight MONOHYDRIC ALCOHOLS.
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8
Q

What are complex lipids. Give examples

A
  • Complex: are esters of fatty acids containing GROUPS in addition to an alcohol and one or more fatty acids. They can exist as; PHOSPHOLIPIDS and GLYCOLIPIDS.
  • > Phospholipids: they contain fatty acids, an alcohol and a phosphoric acid reside.
  • > Glycolipids: also, known as glycosphingolipids. They contain fatty acids, SPHINGOSINE and carbohydrates.
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9
Q

Other forms of lipids such as precursor and derived lipids include (5)

A

fatty acids, glycerol, steroids, other alcohols, fatty aldehydes, ketone bodies

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10
Q

3 types of FA

A
  1. saturated (no DB)
  2. monounsaturated (1 DB)
  3. polyunsaturated (more than 1 DB)
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11
Q

Fatty Acids are named after

A

named after the hydrocarbon with the same number and arrangements of carbon atoms.

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12
Q

Do FAs usually contain even or odd DBs

A

even #

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13
Q

Ending of saturated vs unsaturated

A

Saturated fatty acids end with –anoic and unsaturated fatty acids end with –enoic

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14
Q

Carbon atoms are numbered from the

A

carboxyl carbon (Carbon number 1)

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15
Q

The carbon atoms adjacent to the carboxyl carbon (numbers 2,3 and 4) are also known as the ____
and the terminal methyl carbon is known as ___

A
  • ɑ, β and 𝛄 carbons respectively

- the ω- or n-carbon.

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16
Q

Several conventions use ____ for indicating the number and position of double bonds.

A

Δ

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17
Q

Δ9 indicates that the double bond exists between carbon number ___ of the fatty acid.

A

9 and 10

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18
Q

ω9 indicates a double bond on the

A

ninth carbon counting from the ω-carbon.

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19
Q

In animals, additional double bonds are introduced only between an existing double bond at the _____ position and the carboxyl carbon, this leads to the three series of fatty acids known as ______

A
  1. ω9, ω6 or ω3

2. ω9, ω6, and ω3 families.

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20
Q

Saturated fatty acids: contain ____ double bonds

A

0

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21
Q

Sources of saturated FAs?

A
    • Common name: Palmitic
    • # of C atoms: 16
    • Occurrence: Common in all animal and plant fats
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22
Q

Unsaturated fatty acids: contain ____ double bonds

A

one or more

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23
Q

Unsaturated fatty acids can be divided into what 3 groups

A
  1. Monounsaturated (1 DB)
  2. Polyunsaturated (2 or + DB)
  3. Eicosanoids
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24
Q

What are eicosanoids derived from and the 3 types?

A
  • derived from Eicosa (20-carbon) fatty acids
  1. Prostanoids: such as (Prostaglandins PGs, Thromboxanes TXs).
  2. Leukotrienes (LTs),
  3. Lipoxins (LXs),
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25
Q

What is considered the main storage forms of fatty acids.

A

Triglycerides

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26
Q

What is Cholesterol

A

An AMPHIPATHIC ACID widely distributed in ANIMAL cells. It’s considered the PARENT molecule of all other STEROIDS in the body.

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27
Q

What is lipid peroxidation? (Source of?, caused by? responsible for?)

A
  1. Major source of free radicals
  2. Caused by auto-oxidation of lipids exposed to O2
  3. Responsible for RANCIDITY of FOOD as well as TISSUE DAMAGE in vivo where is can contribute to the pathogenesis of atherosclerosis, cancer, inflammatory diseases and aging.
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28
Q

What are the 3 steps of lipid peroxidation?

A
  1. Initiation
  2. Propagation
  3. Termination.
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29
Q

What are Amphipathic Lipids

A

self-orient at oil/water interfaces to form membranes, micelles, liposomes and emulsions

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30
Q

Example of Amphipathic Lipid

A

phospholipid

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31
Q

What is the fxn of Lipoproteins

A

Lipoproteins transport LIPIDS from the INTESTINE as CHYLOMICRONS and from LIVER as VLDL to most TISSUES for OXIDATION and to ADIPOSE TISSUE for STORAGE

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32
Q

In what form are lipids mobilized from tissues and how can they be transported

A

Lipids are mobilized from adipose tissue as FFA which are bound to proteins e.g. ALBUMIN

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33
Q

What are the Four major lipid classes are present in lipoproteins:

A
  1. Triacylglycerols (16%),
  2. Phospholipids (30%),
  3. Cholesterol (14%),
  4. Cholesterol Esters (36%).
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34
Q

What are the four major groups of lipoproteins? Name their sources, and size

A
  1. Chylomicron
    - Source: Intestine
    - Size: 90-1000nm
  2. VLDL
    - Source: Liver (intestine)
    - Size: 30-90nm
  3. LDL
    - Source: VLDL
    - Size: 20-25 nm
  4. HDL
    - Source: Liver, intestine, VLDL, chylomicrons
    - Size:
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35
Q

List the 4 major groups of lipoproteins in decreasing size

A

Biggest to smallest

Chylomicron -> (Chylomicron remnant) -> VLDL -> LDL -> HDL

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36
Q

List the 4 major groups of lipoproteins in decreasing density

A

Most dense to least dense

HDL -> LDL -> VLDL -> (Chylomicron remnant) -> Chylomicron

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37
Q

What is a lipoprotein core made of? How many layers is the surface of amphipathic lipids and what type of lipids are there?

A
  1. Lipoprotein core is nonpolar consisting of mainly triacylglycerol and cholesterol ester
  2. Single surface layer of amphipathic phospholipid and cholesterol molecules
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38
Q

Which parts of a lipoprotein are hydrophobic vs. hydrophilic

A

Hydrophobic INTERIOR consisting of triacylglycerols and cholesterol esters

Hydrophilic EXTERIOR consisting of cholesterol and phospholipids and apolipoproteins

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39
Q

Role of Apolipoprotein (APO) A-1

A

Activator of the enzyme LCAT (Lecithin Cholesterol Acyltransferase)

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40
Q

Role of Apo B48

A

Chylomicron assembly and secretion by the intestine.

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41
Q

Role of APO B100

A

Low Density Lipoprotein (LDL) particle uptake by extrahepatic cells.

42
Q

Role of APO C-II

A

Activator of the enzyme LPL (Lipoprotein Lipase)

43
Q

Role of APO E3 and APO E4

A

VLDL (Very Low Density Lipoprotein) and Chylomicron remnant uptake by liver cells.

44
Q

Major regulatory role in the metabolism of plasma chylomicrons, VLDL, HDL is via what receptors

A

apo E receptors and LDL receptors

45
Q

What are the 3 common isoforms of apolipoprotein E

A

E2, E3, E4

46
Q

How do the isoforms of apolipoprotein differ

A

differ by AA substitution at one or both of two sites: residues 112 and 158.

47
Q

Discuss the Apolipoprotein E Gene Polymorphism and Risk of CAD, how does each isoform of APO E vary the risk?

A
  • ε4 associated with higher cholesterol levels (~0.2 mmol/L) vs. ε2 associated with lower cholesterol levels (~0.4 mmol/L),
  • Meta-analysis indicted no significant relationship with ε4 and increased CHD risk
  • 4S study indicated an 80% increased risk of dying in MI survivors carrying the ε4 allele
  • Apo E helps to explain differences in inter-population rates of mortality, however, it does not warrant population screening as a risk factor.
48
Q

What is a physical characteristic seen in people with Apolipoprotein E Gene Polymorphism

A

PALMAR XANTHOMA: orangey-brown discoloration of the palm creases

49
Q

Where is liproprotein lipase (LPL) synthesized (3)

A

adipose, heart & skeletal muscle

50
Q

Fxn of LPL

A
  • Hydrolyzes TG in chylomicrons & VLDL

- Transfer phospholipids & apolipoproteins to HDL

51
Q

What does LPL require for activation

A

APO C-II

52
Q

What induces LPL and where is it transported

A

LPL is induced by INSULIN and is transported into LUMINAL SURFACE of capillary ENDOTHELIUM.

53
Q

What is the difference btwn the difference between LCAT and ACAT enzymes.

A

t LCAT synthesize cholesterol esters in the blood for the purpose of lipoprotein trapping. ACAT on the other hand, synthesize cholesterol esters for the purpose of creating storage forms in the cell (and not in the blood).

54
Q

Who is the most important players in reverse cholesterol transport

A

ATP binding cassete A1

55
Q

What is the fxn of ATP binding cassete A1

A

facilitates efflux of free cholesterol and phospholipids to the nascent HDL (APO AI-containing) particles

56
Q

What is the fate of the free cholesterol that is transported by ATP binding cassette A1 onto the nascent HDL particle

A
  • This cholesterol is esterified and the resulting cholesteryl ester then forms the inner part of the spherical HDL particle.
  • Some of the HDL cholesterol is transferred via cholesterol ester transfer protein (CETP) to the LDL particles and ultimately taken up by LDL receptor.
57
Q

Fxn of specific hepatic receptor

A

HDL uptake

58
Q

Discuss the metabolism of HDL in reverse cholesterol transport

A

a

59
Q

About half the cholesterol is made from ____ and the remainder is from ____.

A
  1. Acetyl Co-A

2. diet

60
Q

Write the steps of cholesterol synthesis inc enzymes

A
  1. 2 Acetyl-CoA Acetoacteyl-CoA
  2. Acetoacteyl-CoA HMG CoA
  3. HMG-CoA Mevalonate

EVENTUALLY TO SQUALENE then CHOLESTEROL

61
Q

What is Dyslipoproteinemia

A

Disorders of Plasma Lipoproteins

62
Q

What is an example of Dyslipoproteinemia

A

Familial Chylomicronemia

63
Q

Discuss Familial Chylomicronemia (how is it acquired, what occurs, signs)

A
  • Autosomal recessive inheritance (1 in a million).
  • Decreased or absent LPL activity.
  • > LPL gene mutation (most common)
  • > Apo C-II gene mutation
  • Fasting chylomicronemia and severe elevation in plasma triglyceride.
  • Recurrent episodes of pancreatitis.
  • Hepatosplenomegaly, eruptive xanthomas, and lipemia retinalis (retinal veins/arteries appear white).
  • Chylomicronemia is a rare but important genetic disorder. Interestingly, a number of patients with this disorder have no attacks of pancreatitis.
64
Q

Why is a patient’s plasma likely creamy

A

High TG lvl

65
Q

The figure below shows eruptive xanthomas of the abdomen which is typically seen in patients with _____

A

Lipoprotein Lipase Deficiency.

66
Q

lipemia retinalis which is seen in patients with _____

A

lipemia retinalis which is seen in patients with

67
Q

What are common symptoms of hypercholesterolaemia

A
  • Corneal Arcus (the ring)
  • Xanthelasma (the small eye lid bumps)
  • Xanthoma (bumps)
  • excessive fat buildup and the hardening of the aorta
68
Q

What are possible causes of familial hypercholesterolaemia (FH)? How frequent are these diseases?

A
  1. PCSK9 defects (FH-3).
  2. Cholesteryl ester storage disease (Wolman’s disease).
  3. Familial intrahepatic cholestasis (Alagille syndrome).
  4. Autosomal recessive hypercholesterolemia.
  • These other causes are, with the exception familial defective APO B (the binding of APO B to the LDL receptor is defective resulting in the increase of LDL in blood) are fairly infrequent and occur only in special populations.
69
Q

How does familial hypercholesterolemia present clinically?

A

It presents in a variable fashion. Premature atherosclerosis maybe present.

70
Q

Discuss the mechanism for FH due to defective APO B

A

Decreased LDL catabolism due to impaired interaction of APO B with LDL-R and decreased APO B production.

71
Q

Where is the mutation for defective APO B that causes FH? Is this autosomal dominant or recessive?

A
  • Mutations in exon 26 of the APO B gene,

- Autosomal dominant.

72
Q

What are the clinical manifestation of the FH Phenotype Linked to PCSK 9 Defects (FH3)?

A
  1. Xanthoma tendinosum or other xanthomas, arcus corneae
  2. Premature atherosclerosis
  3. Positive family history.
73
Q

What is the mechanism for FH Phenotype Linked to PCSK 9 Defects (FH3)?

A

Enhanced intracellular degradation of LDL and overproduction of VLDL, IDL and LDL.

74
Q

Where is the mutation for defective APO B that causes FH? Is this autosomal dominant or recessive?

A
  1. PCSK9 is a gain of function mutation,

2. Autosomal co-dominant.

75
Q

What is Hereditary Mixed Hyperlipidemia? Types are Familial Combined Hyperlipidemia (IIa, IIb, IV, NB) or Familial Dysbetalipoproteinemia (Type III)

A

Inherited disorder that causes high cholesterol and high levels of triglycerides in the blood

76
Q

What are the clinical manifestations of Hereditary Mixed Hyperlipidemia

A
  1. Xanthoma tendinosum or other xanthomas, arcus corneae

2. Premature atherosclerosis

77
Q

What is the mechanism for Hereditary Mixed Hyperlipidemia

A
  1. Hepatic overproduction of APO B
  2. Delayed post-prandial chylomicron clearance,
  3. Prolonged post-prandial increase of free fatty acids and APO B-48
78
Q

Where is the mutation for defective APO B that causes FH? Is this autosomal dominant or recessive?

A
  1. Autosomal dominant,
  2. Candidate gene regions:
    - > 1q21-23 (USF10),
    - > 1-q12.1 (A1/C3/A4),
    - > 16q22-24.1 (HDL).
79
Q

What is associated with Familial Dysbetalipoproteinemia (Type III)

A
  1. Homozygous for APO E2 (E2/E2),
  2. Dominant APO E,
  3. Lipoprotein glomerulopathy,
  4. APO E absence (E0/E0),
  5. Hepatic Lipase deficiency.
80
Q

Discuss Familial Combined Hyperlipidemia (autosomal or recesive? signs?)

A
  • Autosomal dominant disorder (1:150),
  • Increased risk of atherosclerosis,
  • No typical physical signs,
  • Changing lipoprotein patterns,
    The “changing lipoprotein patterns: patients may present with either moderately increased LDL cholesterol and triglycerides or only with increases in triglycerides or LDL-cholesterol. However, the hallmark of the disorder is that APO B is always increased.
81
Q

What are the Clinical manifestations of Familial Combined Hyperlipidemia

A
  • Moderately increased cholesterol, triglycerides or both,
  • One-third of affected relatives have elevated TC, 1/3 have elevated TG and 1/3 have elevations of both TC and TG,
  • Increased turnover of plasma APO B,
  • Increased plasma level of APO B.
82
Q

Discuss Dysbetalipoproteinemia: (Type III Disease)

A
  • Frequency is approximately 1:5000,
  • Increased concentration of chylomicron and VLDL remnants (IDL) - β-VLDL,
  • Elevated levels of cholesterol and triglyceride,
    palmar xanthomas, tubero-eruptive xanthomas,
  • Premature coronary artery disease,
  • > 90% of patients are homozygous for the E2 isoform,
  • Additional genetic and/or environmental stimulus required.
83
Q

Discuss Tangier Disease

A
  • Autosomal recessive disorder (~40 patients identified),
  • Enlarged yellow-orange tonsils,
  • Virtual absence of HDL, reduced levels of LDL, moderately elevated triglycerides,
  • Hepatosplenomegaly and peripheral neuropathy,
  • Tangier fibroblasts were defective in removing cellular cholesterol and phospholipids,
  • Evidence of premature CAD.
84
Q

What are the Genetic Defects of HDL Metabolism

A
  1. Tangier disease (ABC-AI defect).
  2. Hypo/analphalipoproteinemia (apo AI defects).
  3. LCAT deficiency (homo/heterozygous).
  4. CETP deficiency (increased HDL-C).
  5. Hepatic lipase defects (increased HDL-C).
85
Q
  • We have already previously described familial sitosterolemia resulting from defective ABCG5 and G8 receptors. Marked increases in HDL occurs in patients with CETP deficiency (where cholesterol is not being transferred from HDL to other lipoprotein particles. The overproduction of lipoprotein(a) does occur in some families and increases the risk of vascular disease.
A

a

86
Q

How does Serum Cholesterol correlates with the incidence of Atherosclerosis and Coronary Heart Disease:

A
  • Elevated plasma cholesterol (>5.2 mmol/L) is one of the most important factors in the pathogenesis of Atherosclerosis.
  • It’s also recognized that elevated levels of Triacylglycerol are an independent risk factor.
  • Any condition associated with prolonged elevation of levels of VLDL, IDL, Chylomicron Remnants, or LDL in the blood are accompanied by premature or more severe atherosclerosis. Examples would be (Diabetes Mellitus and Hyperlipidemia).
87
Q

The above graphs illustrates that there are numerous other studies which indicate the relation between cholesterol and ischemic heart disease is direct, extends to low cholesterol levels and may account for up to 80% of vascular events.

A

a

88
Q

How does Diet can play a role in reducing serum cholesterol:

A
  • Unsaturated FAs can lower the blood cholesterol levels by the upregulation of LDL receptors on the cell surface which will increase the catabolism of LDL which is the main atherogenic lipoprotein.
  • Most people can reduce their cholesterol by btwn 10-30% with diet, but a wide range of responses has been recorded. A case of an 80-year-old man was reported who ate 20 eggs a day for 50 years and still had normal cholesterol levels (clearly a dietary non-responder). Patients with diabetes may over-respond to diet by overproduction of some of the proteins associated with chylomicrons.
  • It appears that individuals whose TGs inc significantly after meals are at greater risk of atherosclerosis than those in whom the increase in triglycerides is small. This may relate to insulin sensitivity (which can be approximated by ratio of triglycerides to HDL).
89
Q

acute vascular events result mostly (but not always) from a rupture of the so-called vulnerable (cholesterol-rich) plaque which is characterized by a thin fibrous cap rupture of which exposes the tissue clotting factor to platelets and leads to the formation of the clot which occludes the artery leading to symptoms of acute myocardial infarction, stroke, etc.

A

a

90
Q

What drug has been proved highly effective in lowering plasma cholesterol and preventing heart disease

A

Statins

91
Q

When oxidized LDL is floating around and macrophages start to phagocytize it, does this mean there is cap on how much oxidized LDL can be brought into the macrophage?

A

a

92
Q

similarities and differences of chylomicrons Vs VLDL:

A

Similarities:

  • Made by an organ,
  • Contains APO B, C, E,
  • Mostly made of triglycerides,
  • Large molecules.

Differences:

  • Chylomicrons are made by the intestine and VLDLs are made by the liver,
  • Chylomicrons have an APO B48 and VLDLs have an APO B100,
  • Chylomicrons contain Cholesterol Esters (CE) and VLDLs contain Cholesterol,
  • Chylomicrons are released into the lymph and VLDLs are released into the blood
93
Q

Review relevant lipids of physiologic significance.

A

a

94
Q

List the major classes of lipoproteins and describe their lipid and apoprotein composition

A

a

95
Q

Discuss lipid metabolism.

A

a

96
Q

List the four lines of evidence linking cholesterol to atherosclerosis.

A

a

97
Q

Differentiate between different forms of dyslipidemias.

A

a

98
Q

Describe the metabolism of lipids (events associated w/digestion and exports of lipids from intestine to lymph) and then when liver releases fat into circulation

A
  1. First we get digestion of large meal that contains lipids. The dietary TG will then initially go thru LYMPATICS in form of NASCENT CHYLOMICRON. Has surface marker of APO-B48. Inside this chylomicron is mainly TG and CHOLESTERYL ESTERS.
    (Previously cholesterol was converted into cholesteryl esters by ACAT)
  2. From lymphatics Chylomicrons move into bloodstream and collide with a HDL. HDL passes on two additional surface markers Apo C and Apo E into the chylomicron. So chylomicron has original Apo-B48, and Apo-C and Apo-E
  3. Eventually when chylomicron reaches into the vicinity of adipocyte it will activate another enzyme called LPL. LDL will breakdown TG and liprotein into FAs. FAs will be transported into adipose tissue and added into a glycerol molecule to generate TGs (FA + glycerol = TG).
  4. The newly formed TGs will be stored in vesicles in adipose tissue and utilized in future for nrg etc.
  5. Since chylomicron has lost some of its TGs, and we’re done activating LPL, the Apo C is given back to HDL, the chylomicron is now a chylomicron reminant. Only has residues of TG, cholesteryl esters, and surface APO E and Apo-B48.
  6. The surface markers Apo-E and Apo-B48 allow chylomicron reminant to bind to surface receptor on liver cell. It will be phagocytosed by liver cell and degraded by lipid enzymes, when we break it down, we release its contents.
  7. The esterase enzyme in liver will take on cholesteryl ester and convert it into cholesterol so get cholesterol stored in liver.
99
Q

Discuss what happens when lipids leave liver (part 2). on Metabolic fate of very low density lipoproteins (VLDL) and production of low-density lipoproteins (LDL).

A
  1. Source of lipids e.g. TGs from liver can come from diet or metabolic pathways e.g. glucose metabolism
  2. Nascent VLDL will leave liver into blood. It has surface markers Apo-B100. Inside VLDL is TGs and cholesterol (NOT cholesteryl esters).
  3. VLDL in the bloodstream collides with HDL molecule that transfers surface marker Apo-C and Apo-E. So it will have ApoB-100, Apo-C, and Apo-E.
  4. Once in the vicinity of adipose tissue, it will activate LPL enzyme. LPL will breakdown TGs into FA, and FA absorbed into adipose tissue, then added to glycerol molecule and TG is regenerated and stored for future use.
  5. VLDL has lost some TG (so shrunk), and will give back Apo-C to an HDL molecule. It still has its original surface ApoB-100 and Apo E. It is now called IDL or VLDL remnant.
  6. IDL has residue TGs, some cholesterol, Apo-E and Apo-B100. IDL has a couple fates. 1) IDL can be taken back into liver and broken down into fragments. 2) Undergo catabolism and cholesterol from IDL can be transferred to HDL molecule, which will convert cholesterol in cholesteryl esters in liver. CE then given back to IDL. 3) Or lose its apo-E and now converted into LDL molecule.
100
Q

Describe how LDL binds to its receptor and what do we do with the cholesterol thats internalized

A
  1. LDL molecule has surface marker ApoB-100 (one copy). LDL will bind to LDL receptor thru recognition of ApoB-100 on surface of LDL particle.
  2. Once LDL binds to receptor, a clathrin-pit forms which helps internalize cholesteryl esters containg LDL thru endocytosis.
  3. LDL receptors will be recycled back onto surface. As we recycle the receptors we tend to lose some of the receptors.
  4. LDL particle will bind to endosome and content will be broken down. Esterase enzyme will convert cholesteryl esters into cholesterols.
  5. Once have unesterfied cholesterol 1 of 4 things can happen.
    - 1) If we have extra cholesterol floating in cell would want to turn off cholesterol synthesis. This is done by blocking rate limiting enzyme in cholesterol synthesis, HMG-CoA reductase.
    - 2) Or activate ACAT enzyme (allows us to make cholesteryl esters which can be stored in cell).
    - 3) Turn off gene expression by which we synthesize new LDL receptors. So once we have extra cholesterol inside the cell, the process by which we make LDL receptors is turned off. So receptors can be down regulated. If not making enough receptors and continuing to lose receptors thru recycling process, then the amt of CE we can bring into cell is limited.
    - 4) Cholesterol can be used to synthesize steroids.

BPK 458 (29 decks)

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