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Cholesterol Transport Flashcards

1
Q

Chylomicrons (CMs)

A

Deliver dietary TGs from intestine —> peripheral tissues

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2
Q

VLDLs

A

Deliver endogenous TGs from liver to peripheral tissues

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3
Q

LDLs

A

Delivers cholesterol from liver to peripheral tissues

Bad cholesterol

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4
Q

HDLs

A

Mediate reverse cholesterol transport from periphery to liver

Good cholesterol

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5
Q

CM higher in TG or cholesterol?

A

TGs

CMs are created in the intestinal epithelial cells during a well-fed state

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6
Q

Lipoprotein lipase (LPL)

A

Tissues that need fFA secrete this enzyme

It is activated by ApoC-II (which is on the CM surface)

Allows the cell to extract FA from the TGs stored in the CM

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7
Q

Where do CM remnants go?

A

After being depleted of its FA stores by peripheral tissues…called remnants

Returned to the liver

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8
Q

In the liver,

TGs and cholesterol are repackaged into what?

A

VLDLs (higher in TG than cholesterol)

Well-fed state: the liver can also synthesize TGs and cholesterol

Fasting state: live can absorb excess FFAs coming from adipocytes, re-esterify them…and package them into VLDLs.

In other words…the liver is ALWAYS making VLDLs —> secreted into the blood

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9
Q

fate of VLDLs remnants (TG-depleted)

A

Returned to the liver to be repackaged again

…

Converted into LDLs (higher in cholesterol than TGs)

—> they deliver cholesterol to the extrahepatic tissues or are taken up by liver to be repackaged again

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10
Q

ApoC-II

A

Tissue source: liver

Lipoprotein distribution: CM, VLDL, IDL, HDL (all except LDL and CM remnant)

Function: activates LDL enzyme

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11
Q

ApoB-100

A

Tissue source: liver

Distribution: VLDL, IDL, LDL

Function:VLDL assembly and secretion, structural protein, ligand for LDL receptor

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12
Q

ApoB-48

A

Tissue source: intestine

Distribution: CM, and CM remnant

Function: assembly and secretion of CMs from the intestinal mucosa

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13
Q

ApoA-1

A

Tissue source: liver and intestine

Distribution: HDL

Function: activates LCAT enzyme, and structural component

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14
Q

ApoE

A

Tissue source: liver

Distribution: CM, CM remnant, VLDL, IDL, HDL (no LDL)

Function: ligand for binding several lipoproteins to…
—> LDL receptor
—> LDL receptor-related protein (LRP)
—> possibly to a separate ApoE receptor

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15
Q

Life cycle of CMs

A
  1. Immature CMs (nascent) are produced in the intestinal epithelium
    —> have ApoB-48 so that it can be assembled
  2. Nascents secreted into the blood
  3. ApoC-II and ApoE are transferred from HDLs they encounter
  4. Cells secrete LDLs, which are activated by Apo-CII and thus degrade the TGs in the CM
  5. ApoC-II is returned to the HDLs
  6. CM remnants (still contain ApoE) bind to receptors on liver and are uptaked into liver
  7. Ultimately redistributed as VLDLs
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16
Q

Fate of VLDL and LDL

A
  1. Liver assembles nascent VLDLs
    —> has ApoB-100
  2. Nascent VLDLs are secreted into the blood and ApoC-II and ApoE are transferred from HDLs encountered
  3. Cell secrete LDLs…activated by ApoC-II (like in CMs) and are depleted of TGs
  4. As getting depleted VLDL —> IDL —> LDL
  5. ApoC-II and ApoE are returned to the HDL
  6. Leaving ApoB-100 as the major apolipoprotein on LDL
  7. ApoB-100 = ligand for LDL endocytosis to deliver cholesterol to tissues
  8. Remaining LDL are taken up by liver via ApoB-100 by same mechanism

Note***VLDL remnants can return to liver to be repackaged via ApoE…or converted to LDLs (#4-5)

  1. LDLs have ApoB-100 which binds to receptors on extrahepatic tissues and liver to mediate uptake —> to deliver cholesterol
17
Q

Receptor-mediated endocytosis of LDLs

A

ApoB-100 = LDL receptor ligand and binds to the receptors

LDL is endocytosed and becomes a endosome

Endosome —> lysosome…and cholesterol is extracted for various uses

18
Q

Cholesterol will regulate its own levels in the cell by which two mechanisms?

A
  1. Shuts down synthesis of cholesterol by inhibiting HMG CoA reductase
  2. Shuts down synthesis of LDL receptors —> inhibits uptake of LDLs
19
Q

Target of statin drugs

A

HMG CoA reductase

20
Q

Cholesterol is (?) for storage

21
Q

Fate of HDL (reverse cholesterol transport)

A
  1. Nascent HDLs made in liver and small intestine
    —> concentrated in phospholipids
    —> low in cholesterol at this point
    —> donates ApoE and ApoC-II to CMs and VLDLs
  2. ApoA-1 activates PCAT/LCAT
  3. PCAT/LCAT grabs cholesterol from the cell suing transporter ABCA1
    —> cholesterol is esterified to one of the FAs of PC
  4. Liver uptakes HDL cholesterol (via scavenger receptor) to be excreted or redistributed
22
Q

OxLDL

A

Enhanced by oxidizing agents: superoxide, nitric oxide, hydrogen peroixde

Anti-oxidizing agents: vitamin E, ascorbic acid, beta-carotene

Can damage the endothelial cells that line blood vessel

Recruits macrophages to damaged cells —> become foam cells —> harden the artery

23
Q

Familial hypercholesterolemia (FH)

General

A

AD

Elevation of plasma LDL

Causes:

  1. Dysfunctional LDL receptor
  2. Increased LDL receptor degradation
  3. ApoB-100 defects reducing receptor affinity

Problems:
1. Premature artherosclerosis and coronary heart disease

24
Q

Heterozygous FH

A

High fasting LDL (250-500 mg/dL)

Normal TGs

CHD onset in 4th-5th decade

Treatment: 1st = statins (inhibit ability to make cholesterol)…statins increase LDL receptor synthesis

2nd = bile acid sequestrants…
—> bile acid is made from cholesterol
—> meds inhibits recycling of bile acids…so have to make more from cholesterol

25
Homozygous FH
Really really high LDL (500-1200) Xanthomas = fatty deposit pockets under skin CHD within 1st 2 decades Unresponsive to statins LDL apheresis to remove ApoB-containing lipoproteins (CM, VLDL, IDL, LDL)
26
Cholesterol ranges
Normal: < 100 mg/dL Near optimal: 130-159 High: 160-189 Very high: >190
27
Familial dysbetalipoproteinemia
High cholesterol and TGs in blood Causes: 1. Deficiency or defective ApoE 2. Unable to clear CM remnant of VLDL remnant Symptoms: 1. Xanthomas 2. Atherosclerosis 3. Angina 4. Peripheral artery disease Treat with low calorie and low fat diets
28
A-betalipoproteinemia
Do not have beta producing lipoprotein complexes = Bassen-Kornzweig Syndrome = microsomal TG transfer protein deficiency (MTTP) Essential for synthesis and secretion of ApoB-48 and 100) Results = no absorption of vitamins ADEK...fat soluble vitamins Symptoms 1. Failure to thrive 2. Diarhhea 3. Star shaped RBCs 4. Fatty stools 5. Cannot balance 6. Vision loss Treatment = fat soluble vitamin supplments...medium chain FAs diet
29
Niemann-pick (Type C) disease
Pertain to the lysosome after LDL receptors are taken up AR Progressive neuro degeneration and lysosomal buildup of cholesterol (and other lipids) in the CNS, liver, and spleen Mutations in NPC1 and NPC2 —> involved in the release of cholesterol from later endosomes and lysosomes after degradation has occurred —> leads to buildup of cholesterol —> feedback inhibition is impaired...no inhibition of synthesis of cholesterola nd LDLr Symptoms: 1. Cant move 2. Hepatomegaly 3. Splenomegaly 4. Jaundice 5. Seizures INBORN ERROR OF METABOLISM - so will see early on in life Treatment = miglustat (new) Prognosis is poor
30
Tangier disease
Rare AR HDL deficiency (ApoA-1) Loss of ABCA1 function Kidneys take over sole function of extract cholesterol - not good at it Cholesterol accumulates in the tissues CM and VLDL do not get ApoC-II from HDLs—> hypertriglycemia Virtually no HDLs of LDLs...but accumulationg of VLDLs Symptoms: 1. Neuropathy 2. Orange-colored tonsils 3. Splenomegaly 4. Corneal clouding 5. Enlarged liver . Type 2 diabetes Treatment = symptomatic and supportive (splenonectomy)
31
Alzheimer’s disease
Cholesterol cannot cross the BBB...must be made and redistributed within teh CNS —> ApoE = main protein that helps to redistribute cholesterol in the CNS —> ApoE can either decrease or increase risk of Alzheimers Isoforms of ApoE: 1. ApoE-2 = may provide protection against the disease...develope it later in life 2. ApoE-3 = most common...neutral role 3. Apo-4 = common, increases risk of developing disease at earlier onset
32
Hypercholesterolemia and CHD
HC increases risk of CHD Treatment aimed to lower total and LDL cholesterol while increasing HDL Want 4:1 (total cholesterol(LDL):HDL ratio) Treatments: 1. Diet, lifestyle changes 2. Statins 3. Bile acid sequestrants 4. Ezetimibe —> blocks cholesterol absorption 5. Niacin and gemfibrozil (decrease TGs, increase HDL cholesterol)
33
Atherogenic dyslipidemia
Combination of 3 abnormalities 1. Increased VLDL TGs 2. Decrease HDL 3. Increased LDL = dyslipidemia profile Associated with: 1. Obesity 2. Metabolic syndrome 3. Insulin resistance 4. Type II diabetes formation 5. Hypertension
34
Smith-lemli-optiz syndrome (SLOS)
Most common genetic defect of cholesterol biosynthesis Defect in 3beta-hydroxysterol-delta7-reductase Results in increased 7-DHC and decreased cholesterol in circulation Morphogenic abnormailies 1. Microcephaly 2. Dysmorphic carniofeatures 3. Polydactyly 4. Congenital heart disease Defects are due to lack of cholesterol to post-translational modification of Hedgehog (Hh) protein With implication in signaling in embyronic patterning

Biochemistry Cardio (13 decks)

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