26. Lipids & Lipoproteins Flashcards

1
Q

How are isoprenoids formed

A

3 acetyl CoA —> isopentenyl pyrophos (IPP) = which are building blocs for isoprenoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the sources of acetyl CoA

A

Oxidative decarbox of pyruvate

betaa ox of FA

Breakdown of AA

(All in mitochondria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the structure of cholesterol

A

Alicyclic compound w/ 27 Cs

-sterane ring, 8 C hydrocarbon, 2 methyl groups, 1 double bond and 1 -OH group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what compounds is cholesterol a precursor for

A

bile acirs & bile salts

vit D

steroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the rate limiting step for cholesterol synthesis

A

HMG CoA reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what can IPP form

A

steroids

lipid soluble vitamins

others like ubiquinone & lipid anchors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what inhibits the conversion of lanosterol to cholesterol

A

antifungal agents (miconazole)

tamoxifen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what medications inhibit HMG CoA reductase

A

statins (comp inhibitor)

-which have higher affinity than the natural molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why do statins have myotoxic side effects

A

also end up inhibiting the formation of ubiquinone –> impair mitochondria fxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the “fate” of cholesterol

A

cholesterol esterfied by ACAT

packaged inot VLDL & released into blood

& more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what happens to cholesterol formation in fed state

A

reduced bc glucagon inhibits HMG CoA by phosphorylating it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what happens to transcription with low sterol

A

promote release of SREBP-SCAP from ER to golgi –>

proteolysis and release mature SREBP to dimerize & translocate to nucleus –>

binds to SRE and promotes transcription of HMG CoA Reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are lipoproteins

A

vehicles for transport of cholesterol, cholesterol esters, TAGs, & fat soluble Vits

=chylomicrons, VLDL, IDL, LDL, HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how do lipoproteins contribute to lipid metabolism

A
  1. transport and deliver TAGs
  2. cholesterol homeostasis by transporting it to liver
  3. apolipoprotein –> target signals/ligands to internalize receptors
  4. apolipoproteins–> activate enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what cell markers do chylomicrons have and what are the fxns

A

ApoB-48 - facilitate transport

ApoC-II - activate cap lipoprotein lipase (CLPL)

ApoE - facilitates uptate into liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the biomarkers on VLDL, IDL & LDL

A

VLDL - ApoB-100, ApoC-II, ApoE

IDL - ApoB-100, ApoE

LDL- ApoB-100

17
Q

what biomarkers are on HDL & what are their fxns

A

ApoA-I - activate enzyme that esterfy cholesterol

ApoC-II -activate CLPL

ApoE - promote uptake into liver

18
Q

what are the steps of processing chylomicrons

A
  1. immature chylomicrons (dietary lipids) in SI travel thru blood
  2. HDL donate ApoC-II & ApoE –> mature
  3. CPLP hydrolyze TAG into glycerol & FFA (release ApoC
  4. remaining endocytosed by liver - bind ApoE
19
Q

explain the processing of VLDL, IDL & LDL

A
  1. VLDL made in liver –> blood
  2. CLPL hydrolyze TAG into glycerol & FA (release ApoC-II) –> IDL
  3. IDL deliverd to liver (use ApoE) & lose more TAGs & ApoE –> LD
  4. LDL deliver cholesterol to liver and peripheral tissue using ApoB-100
20
Q

what is the uptake mechanism for LDL

A

ApoB-100 bind target cell –>

internalize into cell –> make vesicle –>

decrease pH in vescile –> LDL seperates out –>

send to lysosome for breakdown –> get cholesterol & AA

21
Q

What are the steps for the processing of HDL

A
  1. immature disc shaped HDL made in liver & SI
  2. pick up cholesteol from peripheral tissues
  3. LCAT esterfy cholesterol –> cholesterol ester enter HDL core
  4. HDL donates and receives ApoC-II & ApoE, transfer esters to VLDL, IDL & LDL & deliver cholesterol to liver
22
Q

what are the benefits of HDL

A

reduce risk fo CAD

  • reverse cholesterol transport - take up cholesterol from tissues and deliver to liver for excretio
  • antioxidant, anti-inflam, anti-throm & NO inducing
  • inhibit oxidation of LDL
23
Q

what occurs with ABCA1 mutation

A

inactivate cholestrol-transport protein in endothelial cells & macrophages

unable to transport LDL –> accumulate cholesterol in macrophage –> premature athresclerosis

=Tangier disease

24
Q

what increases HDL

A

exercise

weight loss

quitting smoking

25
Q

What is type I hyperlipoproteinemia

A

inability to hydrolyze TAG in chylomicron & VLDL

-deficient CLPL (infants) or ApoC-II (teens)

TAG > 1000 mg/dL –> cream color in blood sample

present with abd pain, acure pancreatitis, cutaneous eruptive xanthomas

26
Q

What is type II hyperlipoproteinemia

A

familial hypercholesterolemia

deficient LDL receptor (cant recognize ApoC 100) –> increase cholesterol in blood –> oxidize LDL –> inflam response –> artherosclerosis

symptoms: xanthomas, angina pectoris

27
Q

how does atherosclerosis form

A

LDL-C accumulate –> oxidize –> accumulate in vessel wall –>

endothelial injury –> influz of LDL into arterial wall

–> inflam response from oxLDL –> macrophages become foams cells –> form plaques