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CPR Exam 1 > Lipids And Lipoproteins > Flashcards

Lipids And Lipoproteins Flashcards

1
Q

How to make isoprenoids (IPP) and its significance

A 
3 acetyl CoAs 
Precursor for
- steroids (cholesterol)
- Lipid vitamins 
-ubiquinone
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2
Q

How does Acetyl Co A get into cytoplasm

A

Citrate shuttle

Made from pyruvate, aa, FAs in mitochondria

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3
Q

6 units of IPP forms

A

Tetracyclic sterane ring

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4
Q

Cholesterol is allicyclic meaning

A

OH at 3rd position

Hydrophobic and hydrophilic

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5
Q

Cholesterol is precursor for

A

VIT D
Bile
Steroid hormones (E, P, Cortisol, Aldosteron, T)

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6
Q

Breakdown of cholesterol

A

No enzymes Can only be excreted by in liver

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7
Q

Daily cholesterol recommended intake and how much body makes

A

<300mg

0.75g-1.0g / day

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8
Q

Synthesis of cholesterol needs what

A

18 ATP
18 Acetyl CoA
16 NADPH

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9
Q

Phase 1 of cholesterol synthesis

A

3 AcetylCoA ——> IPP
2 Acetyl CoA (acetoacetyl CoA)—HMG CoA synthase—> HMG CoA
RLS : HMG CoA reductase (HMG CoA—> Mevalonate)

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10
Q

Phase 2 of cholesterol synthesis

A

IPP ——> Cholesterol

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11
Q

How is HMG CoA reductase functioning

A

Made in ER

Catalytic domain is on cytosolic side (where statins or HMG CoA binds)

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12
Q

Inhibiting IPP synthesis by Statin can also inhibit what synthesis

A

Heme A
Ras protein
Ubiquinone
Dolichol

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13
Q

Statin is what kind of inhibitor
Affinity
+ side effect of long term use
- side effects

A

Competitive inhibitor
Higher affinity
Transcription of LDL receptor for cells to take up cholesterol
Myotoxic: X ubiquinone——> fatigue and muscle death

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14
Q

Direct and covalent modification to regulate HMG CoA Reductase

A

Direct : FFA, bile, oxysterol, statin
Covalent Modification : Phospholylation = inactivates, dephosphorylated = activated
* low energy = high AMP —> AMPK activated = phosphorylates it

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15
Q

What dephosphorylates or phosphorylates HMG CoA Reductase

A

Phosphorylates: AMPK + Glucagon

Dephosphorylates : Insulin

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16
Q

What can increase translation of HMG CoA Reductase

A

VIT E

17
Q

HMG CoA Reductase TF and gene

A

SREBP (binds to SRE on promoter)

  • low cholesterol or on statin use : protease (SCAP) cuts of SREBP and it goes to Golgi —> Nucleus to activate SER on promoter
  • high cholesterol : INSIG keeps SREBP-SRE in ER
18
Q

Lipoproteins function

A

Transport cholesterol, fat, VIT

  1. Deliver TAGs from liver + GI to tissues
  2. Deliver Cholesterol to liver for excretion
  3. Activate enzymes for lipid metabolism
19
Q

5 times fo Lipoproteins

A 
Chylomicrons (biggest + lowest density)
LDL
HDL (smallest + highest density)
IDL
VLDL (second largest)
20
Q

Chylomicrons vs HDL

A

Chylomicrons have a lot of TAGs

HDL has a lot of protein

21
Q

Where are chylomicrons made

And composition

A

In intestinal cells
(From fat we eat)
Largest, lowest density,, highest TAGs
* has ApoB-48 : protein to help transport it
*ApoE : uptake to liver
*ApoC : activates capillary lipoprotein lipase to break it

22
Q

Where are VLDL made

And composition

A

In liver
ApoC : activate capillary lipoprotein lipase
ApoE : uptake to liver
ApoB-100 : uptake into cells

23
Q

IDL and LDL composition

A

IDL : ApoB-100 + ApoE

LDL : ApoB-100

24
Q

LDL has high

A

Cholesterol

25
Q

HDL composition

A

Smallest, most dense, high protein + phospholipids
ApoC
ApoE
ApoA- 1 : activates enzyme to esterify cholesterol

26
Q

Chylomicron Processing

A
  1. Made in SI + package dietary fats
  2. Go into lymph and BV : Nascent Chylomicron (ApoB-48)
  3. Mature Chylomicron : ApoB-48 +ApoE + ApoC
  4. ApoC is released and = Chylomicron remanent —> goes into liver*
27
Q

Hyperlipoproteinemia Type 1 (familial hyperchylomicronemia)

A

X ApoC (adolescent) OR lipoprotein lipase(primary, in infancy) : no capillary lipoprotein lipase made to get fats into blood or tissues for exchange from the Chylomicron
Sx: Xanthomas
TX : low fat diet

28
Q

Hyperlipoproteinemia Type 2

A

X ApoB-100 recognition : no uptake of fats
X LDL receptor *
Sx: dies form CAD (if homozygous) , Xanthomas

29
Q

VLDL processing

A
  1. Made in liver and release into Blood stream (ApoB-100,ApoE, ApoC)
  2. Capillary LPL hydrolysis of glycerol to FFAs
  3. ApoC released = IDL *
30
Q

IDL fate

A
  1. IDL can enter liver to release FFA in liver or stay in blood
  2. IDL looses a lot of TAGs in liver and other tissues and looses ApoE = LDL*
31
Q

LDL fate

A
  1. LDL delivers cholesterol to liver and other tissues with ApoB-100 binding to LDL receptor (brings cholesterol into cells)
    * if too much it stays in BV and makes plaques
32
Q

LDL is taken up to tissues by

A

Receptor- mediated Endocytosis
ApoB-100 binding to LDL receptors
LDL degraded by lysosome —> Cholesterol

33
Q

Familial hypercholesterolemia

A

LDL receptors are unable to release the LDL bound to them

Mutated LDL receptors

34
Q

HDL processing

A
  1. Made in SI and liver as nascent HDL released in blood
  2. They pick up cholesterol from tissues (ApoA-1)
  3. LCAT : esterify cholesterol inside = mature HDL *
35
Q

Other functions of HDL

A
  1. Provide Chylomicron with ApoE and ApoC * (Chylomicron maturation)
  2. Exchanges TAGS, cholesterol, cholesterol esters with LDL, IDL, VLDL
    * takes all esterified cholesterols to liver for excretion
  3. Antioxidant, higher by exercise and weight loss, anti-diabetic
36
Q

ABCA1
Function
Loss of it causes

A 
Transport protein that ApoA-1 binds to (of HDL) and transports LDL
Tangier Disease (HDL deficiency and high cholesterol)
37
Q

What happens with excess LDL

A

Oxidized to oxLDL which is deposited in the BVs

= injury = inflammatory response = macrophages become foam cells = platelet adhesion + SM recruited = bigger plaque

CPR Exam 1 (20 decks)

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