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Clinical biochem. > Lipoproteins > Flashcards

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

A

LDL

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
Q

Describe the condition: familial hypercholesterolaemia

A
  • 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
Q

Describe the condition: Hyperlipidemia (hyperprotenemia)

A
  • Inc. TG OR Inc. Chol.

- elevated lipoproteins OR lipids (Both = combined/familial hyperlipidemia/Hyperlipoproteinemia)

27
Q

Describe the reverse indirect pathway which is mediated by _ & function

A

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
Q

describe the exogenous cycle: chylomicron metabolism

(eating)

A
  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
Q

Describe the endogenous lipid transport cycle (fasting)

A
  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
Q

describe hypertriglyceridaemia & cause

A
  • inc. TG, VLDL (not LDL)

- bc deficiency of LPL or over production of VLDL

31
Q

Describe the reverse direct pathway when there is a lot of cholesterol in tissues (need to be excreted)

A
  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)

Clinical biochem. (12 decks)

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