Lipid Flashcards

(46 cards)

1
Q

whats the function of cholesterol?

A

1- structure of membranes

2- precursor of steroid hormones and bile acids

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2
Q

where do you get most of the cholesterol ?

A

synthesized de novo

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3
Q

how are lipids and cholesterol transported within the body?

A

lipoproteins

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4
Q

whats the basic structure of cholesterol ?

A

4 rings

polar head pointing outside

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5
Q

whats does the 4 rings do?

A

increase fluidity

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6
Q

whats the function of polar head?

A

ester bond forming

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7
Q

whats the form of cholesterol that is running in your body

A

cholesterol ester form ( 2 cholesterol bond by ester bond )

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8
Q

whats the substrate of cholesterol ?

A

acetyl coa

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9
Q

whats the cofactor that is used?

A

NADPH –> anabolic

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10
Q

what are the steps in byiosynthesis of cholesterol?

A

2 acetyl coa —> HMG COA —-> mevalonate —>IPP —> squalene –> cholesterol

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11
Q

whats the enzyme that is responsible for combining the 2 acetyl
coa

A

thiolase

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12
Q

whats enzyme responsible for converting acetoacyle coa ( 2 acetyl coa ) to HMG COA

A

HMG COA synthase

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13
Q

whats the enzyme responsible for converting HMG COA into mevalonate?

A

HMG COA REDUCTASE

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14
Q

whats the main limiting STEP and the one regulating cholesterol synthesis?

A

HMG coa —-> mevalonate

by HMG REDUCTASE

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15
Q

what cofactor does HMG coa reductase need?

A

NADPH

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16
Q

whats the short regulation of HMG coa reductase?

A

phosphorylation of the enzyme :

if you add phosphate it will become inhibited and inactive

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17
Q

whats the kinase that is responsible for the short term regulation?

A

AMP dependent protein kinase

its active in AMP ( low energy state ) and it will inhibit HMG COA reductase by phosphorylation it , because we dont have energy to produce cholesterol

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18
Q

whats long term regulation of HMG COA ?

A

degradation and formation of the enzyme itself

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19
Q

what could lead to degradation of HMG coa ?

A

cholesterol negative feedback

20
Q

whats the transmembrane in the HMG COA that is responsible for the degradation?

A

sterol sensing domain

21
Q

whats the enzyme responsible for forming ester bonds between cholesterol ?

A

ACAT ( intracelluar )

22
Q

whats the enzyme responsible for forming ester bonds between cholesterol EXTRACELLUAR ?

23
Q

can we degrade cholesterol?

24
Q

whats the fate of cholesterol?

A

converted into bile acids and is secreted in bile

25
whats lipoprotiens?
particles found in plasma that transport lipids including cholesterol
26
what are the 5 examples of lipoproteins ?
Chylomicrons ( largest , lowest in density ) VLDL IDL LDL HDL ( smallest but highest in density ) AS YOU GO DOWN YOU LOSE TRIGLYERICDES
27
which apo protein is found in lipoproteins made by intestine?
B48
28
which apo protein is found in lipoproteins made by liver?
b100
29
which lipoprotein has the highest compositon of triglycerides and lowest cholesterol?
chylomicrons
30
which lipoprotein has the highest composition of cholesterol ?
LDL
31
which lipoprotein has the highest protein composition ?
HDL
32
which lipoprotein has apo protein b48
chylomicrons because its formed in the intestine
33
which lipoprotein has apo protein b100
VLDL cuz its made in the liver IDL LDL
34
under which circumstances you cant find chylomicros in plasma?
fasting for 12 hours after a meal
35
describe the cycle of chylomicrons?
AFTER A MEAL 1- small intestine will collect both cholesterol and triglycerides and surrounds them with APPO PROTEIN B48 2- HDL gives the chylomicron APO C 2 AND APO E 3- chylomicrons travel in the blood until it reaches the liver 4- during the travel , LIPOPROTEIN LIPASE WILL BE ACTIVATED BY APO C WHICH WILL BREAD TRIGYLCERIDE FOR STORAGE 5- when it reaches the liver most of the triglycerides will be gone and only cholesterol will be there 6- before it enters the liver it will give HDL apo C2 BACK 7- Chylomicrons remimant will be reach the liver and it will be RECOGNIZED VIA APO E AND IT MEDIATES THE UPTAKE
36
whats the function of apo c2?
activation of lipoprotein lipase and degradation of TRIglycerides
37
whats the function of apo E?
its helps the liver uptake chylomicrons remnant
38
describe the cycle of VLDL, IDL, LDL?
in the liver there will be 3 sources of cholesterol : one is from the chylomicrons coming with cholesterol only ( remember the triglycerides where taken by lipoprotein lipase ) one is from the de novo the liver synthesis cholesterol one is from adipose tissue so what does the liver do? it combines all of them and covers them with APO B 100 forming : VLDL 1- VLDL will leave the liver with only APO B 100 2- HDL will give VLDL apo c2 and apo E --> VLDL WILL HAVE APO B 100 + APO C2 + APO E 3- while VLDL travel in the blood stream , APO C2 will activate lipoprotein lipase and it will start degrading triglycerides like in the chylomicrons scenario 4- after losing bit of triglycerides it will become IDL 5- IDL ( apo b100 + Apo c2 + apo E) will give back APO C2 AND APO E back to the HDL 6- after giving back the apo proteins it will become LDL 7- LDL ( only have apo b 100) is mostly formed of cholesterol and it cant be degraded so it will have options either : GO BACK TO THE LIVER FOR HELP VIA LDL RECEPTOR DEPOSIT THE CHOLESTEROL IN ENDOTHELIUM AND CAUSE ATHEROSCLEROSIS
39
whats the function of LDL receptor?
it will make the liver endocytose LDL
40
what does the liver does when it has soo much cholesteorl?
1- Stops synthesis 2- LDL receptors endocytosis 3- Starts storing the already formed the cholesterol ( ACAT)
41
Describe HDL?
its formed by the body to take the deposited cholesterol and free cholesterol from tissue back to the liver ( good thing )
42
whats are other functions of HDL
- transfer cholesterol back to the liver - give proteins to the other lipoproteins -convert cholesterol to cholesterol ester via LCAT ( EXTRACEULLAR )
43
how does HDL give other lipoproteins the apo proteins
CETP enzyme cholesterol ester transfer protein
44
whats lipoprotein a?
LDL that has apo a that is bound to apo b100 disulfide linkage
45
whats the function of lipoprotein A?
unknown
46
whats risk associated with Lipoprotein A
premature coronary artery disease and stroke