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BIOCHEM - 2ND YEAR > seminar week 1 - SS > Flashcards

seminar week 1 - SS Flashcards

1
Q

What are lipoproteins and the funciton

A
  • Spherical macromolecular complexes.
  • help transport pf lipids through blood stream betweem tissues- TAG, Cholestrol ester, cholestrol, fat-soluble vitamons)
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2
Q

general structure of lipoproteins

A
  • non polar core: mostly TAG and cholestrol ester
  • single surface layer amphipathic lipids: phospho and cholestrol
  • protein moiety of lipoprotein=apolipoprotein or apoprotein
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3
Q

classification of LPP according to
a) denisty
b) electrophoretic mobilities
LOW TO HIGH

A

a: chylomikrony, VLDL, IDL, LDL, HDL
b: chylomricon, LDL, VLDL, HDL

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4
Q

Class of LPP according to
a. triacylglycerol
b. choelstrol
c.phospholipid
d. proteins

LOW TO HIGH

A

a. HDL-LDL-VLDL-CHOLYMIKRON
b. CHOLY-VLDL-HDL-LDL
c. CHYLO-VLDL-LDL-HDL
d. CHYLO-VLDL-LDL-HDL

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5
Q

what are the functions of apoproteins

A
  1. form part of structure of lipoprotein(apoB, struc comp of VLDL and chylo)
  2. enzyme cofactors(apoC-11 doe LPP lipase, apoA-1 doe lecithin: cholestrol acyl transferase (LCAT), enzyme inhibitors like apo a-2 and apo c3 for lipase)
  3. act as ligands for interaction with lipoprotein receptors in tissues(apoB-100 and apoE for LDL receptor, apo-1 for HDL receptor)
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6
Q

Function of Chylomicrons and its assembly

A

function: transport of all dieatry lipids into circulation

assembly:
- intestinal mucosal cells
- carry dietayr(Exogenous ) TAG, chole, fat soluble vit and esters–>peripheral tissues

  1. apoliprotein synthesis:
    - apo B-48 in RER
    - long chain esterified–>yield TAG in mucosal cells and with other dietary thing–>incorportaed into LP in SER
  2. assembly of apolipoproteins and lipids–>chylo: need microsomal TAG trasnfer protein
    - secretory vesicles–>exocytosis
  3. lymphatic sys –>syst circulation
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7
Q

what is nascent CM modification

A
  • incomplete
  • receive apoE and apoC-II from HDL
  • Apoc-11–>act LPL
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8
Q

degradation of TAG by LPL

A

LPL: extracellular enzume, anchored by heparan sulfate. Hydrolyzes TAG in CM –>FFA +glycerol.
- FFA stored
-glycerol used by liver

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9
Q

what happens with the CM remnants: formation and digestion

A
  • apoC-11 –>HDL
  • remnant remove dby liver
  • CM remnants bind to receptors–>apo e–>hepatocytes by endocytosis. –>lysosome, apoproteins and cholestryl esters and other components are hydrolytically degraded–>AA, chol, FFA
  • Free CH -de novo CH stnthesis in liver(allosterid inhibition of HMG-coa red and lowwe the enzyme cell content)
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10
Q

VLDL function and release

A

function: carry lipids from liver to peripheral tissus

release:
-apoB-100 in RER
- secreted–>blood bt liver as nascent VLDL. contain: TAG, choelstrol, cholestrol estera and phospholipid apob-100 , apoA-1

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11
Q

Modification of circulating VLDL

A
  • apoC-2+apoE + VLDL form HDL
  • TAG degreaded by LPL–>VLDL smaller
  • apoC-2 and E–>HDL
  • some TAG from VLDL–>HDL, same time as cholesttryl ester from HDL–>VLDL by CEPT
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12
Q

LDL production from VLDL in plasma

A
  • Formation of VLDL remnants or intermediate-density lipoprotein(IDL)
  • IDL: liver via LDL(apoB-100, E) receptor, or converted to LDL
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13
Q

LDL function and formation

A

function: transport choelstrol to the peripheral tissues(or return it to the liver)

formation
- from VLDL via IDL in plasma, contain apoB-100
- high con of choelstrol and esters, less TAG
- bind to LDL receptors(apoB-100(apo E receptors
- LDL

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14
Q

LDL : receptor mediated endocytosis

A
  • LDL receptors: neg charhed glycoproteins clustered on membranes
  • intracellular side: protein clathrin-stabilizises
  • binding–>endocytosis–>endosomes
    ph falls–>sep of LDL from receptor
  • receptors recycled
    lipoprotein remnants –>lysosome–Zlysosomal enzymes–>chol, aa, FA and phos
  • reutilized
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15
Q

effect of endocytosed choelstrol on cell cholestrol content

A

nhibition of HMG-CoA reductase (cholesterol derived from CM, HDL, LDL)
* ECH formation – ACAT ( acyl-CoA cholesterol acyltransferase)
* low of LDL receptor synthesis

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16
Q

what participate in formation of atherosclerotic plaque

A

In addition to the highly specific and regulated LDL-mediated pathway,
scavenger receptor class A (SR-A) of macrophages, can bind oxidized LDL.
* Cholesterol esters accumulate in macrophages and cause their transformation
into “foam” cells, which participate in the formation of atherosclerotic plaque.

17
Q

HDL function and formation

A

function: reverse cholestrol transport-from peripheral tissues to liver
- acr as repository for apoC-2 and apoE required in metabolism of CM and VLDL

fromation
- syntehsized and secreted from liver and intestine
- apoC-2 and apoE: in liver: form liver HDL–>interstinal HDL when in plasma
- nascent HDL: discoid phospholipid bilayer with apo A and free chol

18
Q

HDL uptake of free CH

A
  • Reverse cholestrol trabsport: atp-bidning casette transportter A1(ABCA1)
    - hydrolysis of ATP to binding of substrae: cant cross membrane.
    - it transfer chol from cell–>poorly lipiated particles like pre-HDL or apo A-1–>HDL3
19
Q

Esterification of free CH

A
  • cholestrol taken up by HDL–>esterified by LCAT
  • LCAT and apo A-1 bidn to discoidal particles=> phos + free chol–>cholestryl esters+lysolechitim
  • ninpolar choelstryl ester–>int bilareye
  • lysolecthin–>plasma albumin
  • nacent HDL–>poor HDL3 then HDL2 which carry esters to liver
  • SR-B1 mediate uptake, it binds to HDL
20
Q

Referance values of
- TCH
- HDL
-LDL
-TAG

A

TCH (total cholesterol)  5,17 mmol/l

HDL >1,03-2,00 mmol/l men
>1,20-2,20 mmol/l women

LDL < 3,4 mmol/l = TCH – (TAG/2.2 + HDL)
 if TAG < 4.6 mmol/l

TAG 0,4-1,7 mmol/l

TCH = LDL + VLDL + HDL + C

Index parameters
TCH/HDL < 5.2
LDL/HDL < 3.5

21
Q

DiSsorder of plasma LP metabolism-Dyslipoproteinemias
what types do we have

A

Primary: independant, geneteically
secondary: consequence

22
Q

most common primary HLP

A

Familiar hypercholestrolemia (FH)
- Mutation in the LDLR gene(chr 19)
-increase of plasma CH depends on the type of mutation, and hetero or homozygosity(gene dosage effect)
- conseqeunces: skin xantomas and tendon xantelasma, arcus cornea, premature atherosclerosis

23
Q

secondary DLP

A
  • by other primary disease
  • cardiovascular system is same
  • treatment: primary disease and hypolipidemic drugs
  • responds to dietary intervention

BIOCHEM - 2ND YEAR (8 decks)

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