Lipoproteins Flashcards

1
Q

Cholesterol is stored in the _ (organ) as _ (name) by _(enzyme)

A

a. Liver
b. Cholesteryl-ester (ester form is more fat soluble)
c. LCAT

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2
Q

ampiphatic meaning. & e.g

A

molecule that is hydrophilic & hydrophobic

e.g. phospholipid

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3
Q

The name of cholesterol transporters. & the types from biggest to smallest (& dec. fat; inc. protein & inc density)

A

lipoprotiens

  1. chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
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4
Q

what’s the apoprotein (apo) of HDL & receptor which helps cells recognise HDL

A
  1. Apo-A1

2. ABCA1

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5
Q

How can cholesterol transfer from lipoprotein to cell (which needs it)?

A

When apoprotein (apo) on lipoprotein matches w/ a receptor on cell

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6
Q

what’s the apoprotein (apo) of LDL

A

Apo-B-100

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7
Q

4 ways cholesterol is used in the body

A
  • Component of cell and organelle membranes
  • Precursor for steroid hormones
  • Precursor for vitamin D
  • Precursor for synthesis of bile acids and salts
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8
Q

_ occupies most of the volume of adipocytes.

A

Cholesterol

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9
Q

where can cholesterol be found

A

inside, outside & within body

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10
Q

The outer layer of the cell membrane contains (a), which is fat soluble and it is transported through the blood in the form of water-soluble carrier molecules using (b) as carriers

A

a. Cholesterol

b. Lipoproteins

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11
Q

Lipoproteins consist of:

A
  • Cholesterol
  • Phospholipids
  • Proteins
  • Triglyceride
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12
Q

functions of apolipoproteins

A
  • mediate binding of lipoproteins w/ lipoprotein receptors
  • required for synthesis of lipoproteins
  • Co-factors for enzymes
  • synthesis, secretion & catabolism of lipoproteins
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13
Q

LDL vs HDL: what they do

A
  • LDL: distributes cholesterol from liver to peripheral tissues
  • HDL: takes cholesterol from peripheral tissues to liver
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14
Q

what is LPL & function of LPL (lipoprotein lipase)

A

a) glycoprotein present on all cells
b) - breakdown TG (-> then carried by apo/lipoprotein)
- excess LPL > protects body from obesity
- deficiency LPL > bad = accumulation of chylomicron-TG in plasma

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15
Q

describe LPLD

A
  • LPL deficiency => elevates fat in blood
  • rare genetic cond.
  • Glybera: 1st gene therapy > remedy for LPLD
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16
Q

affect of insulin on adipocytes & skeletal muscles in relation to LPL

A
  • adipocytes activated to produce & secrete LPL

- skeletal muscle inhibit secretion of LPL

17
Q

which carrier carries ~ 2/3 of Cholesterol in plasma

18
Q

How is cholesterol in LDL taken up by the liver (hepatocytes)? & affect of excess LDL

A
  1. LDL binds to LDL receptor on hepatocyte
  2. LDL endocytosed by clathrin
  3. LDL hydrolysed to AA, FA & cholesterol
  4. cholesterol converted into chosteryl ester via LCAT
  5. LDL receptor can go back to cell surface
    * NOTE: excess LDL could inhibit LDL receptor
19
Q

How does cholesterol bind to HDL form HDLc

A
  1. cAMP activates Protein kinase A
  2. phosphorylation => conformatioinal change => ATP can bind
  3. opens channel => cholesterol can bind to HDL
20
Q

Function of Statin or HMG-CoA reductase inhibitors

A

cholesterol lowering drugs that inhibit the enzyme HMG-CoA reductase - produce cholesterol
=> low cholesterol = prevent CVD

21
Q

limitations to Friedewald equation

A
  • chylomicrons present
  • TG > 400 mg/dL (4.52mM)
  • patients w/ type III hyperlipoproteinemia
22
Q

atherogenic cholesterols

A
  • LDL & VLDL & IDL

all except HDL

23
Q

The equation used for calculation of non-HDLc =

A

non-HDLc = Tc - HDLc

24
Q

explain Tangier disease

A
  • Hypolipoproteinemia / Hypolipidemia
  • absence of the transporter ABCA1 transporter => accumulation of cholesterol in the cell = low cholesterol and HDL in serum.
25
Describe the condition: familial hypercholesterolaemia
- primary disorder of lipoprotein metabolism (hyperlipidaemia) - Inc. LDLc in blood - *defects in LDL receptor (bc mutations) = not absorb LDL - OR excess production of LDL - OR ApoB100 is faulty
26
Describe the condition: Hyperlipidemia (hyperprotenemia)
- Inc. TG OR Inc. Chol. | - elevated lipoproteins OR lipids (Both = combined/familial hyperlipidemia/Hyperlipoproteinemia)
27
Describe the reverse indirect pathway which is mediated by _ & function
a. cholesteryl ester transfer protein (CETP) > exchanges TG in VLDL for cholesteryl esters in HDL b. 1. VLDL processed to LDL => removed from circulation by LDL receptor pathway 2. TG in HDL degraded by hepatic lipase => small HDL particles => uptake of cholesterol from cells
28
describe the exogenous cycle: chylomicron metabolism | (eating)
1. TG & chol. from broken-down food is absorbed in the small intestine 2. lipids are transported in chylomicron 3. LPL breaks down chylomicron to VLDL & FFA -> goes to muscles & adipocytes 4. VLDL goes to the liver
29
Describe the endogenous lipid transport cycle (fasting)
1. liver produces VLDL 2. VLDL (carry TG, Chol.) is broken down by LPL from tiss. => remove FFA &TG (to muscle, adipocytes) 3. this reduces the size of VLDL -> IDL -> LDL
30
describe hypertriglyceridaemia & cause
- inc. TG, VLDL (not LDL) | - bc deficiency of LPL or over production of VLDL
31
Describe the reverse direct pathway when there is a lot of cholesterol in tissues (need to be excreted)
1. Cholesterol in tissue taken up by HDL 2. LCAT converts cholesterol to cholesteryl ester 3. liver uptakes cholesteryl ester in via SR-BI (reverse scavenger)