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CPR I > Lipids and Lipoproteins > Flashcards

Lipids and Lipoproteins Flashcards

1
Q

What makes isoprenoids?
What is that made of?
What do isoprenoids make?

A

one isopentenyl pyrophosphate (IPP)
Three acetyl CoA
steroids, lipid-soluble vitamins, ubiquinone, and prenyl groups t

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2
Q

sources of acetyl coa?

A

oxidative decarbo of pyruvate, beta oxi of fatty acids, breakdown of aa
transport citrate shuttle

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3
Q

cholesterol is made of

A

sterane (allicyclic)
2 (a-coa) -> 27 c (w/ atp to make)
in plasma mem, so has OH

in bile acids/salts/ vit d/ steroid hormones
made and ingested, recycled or peed out

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4
Q

phase 1 - cholesterol synthesis

A

a-coa -> acetoacetyl coa + hmg-coa synthase -> hmg coa + HMGCOA REDUCTASE -> mevalonate -> isopentenyl pyrophasphate (IPP)

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5
Q

rate lim of cholesterol syn? what inhibits this, and what else does it affect?

A

HMG-COA REDUCTASE

inhibited by statin which can inhibit the making of lipid soluble vit, ubiquinone

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6
Q

phase II of cs

A

6 IPP -> squalene (open chain)-> lanosterol (cylic)-> cholesterol

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7
Q

what inhibits phase ii

A

antifungal agents - azoles, tamoxidfen (breast ca drug)

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8
Q

which has a higher affnity for the substrate - HMG-CoA reductase or statin? What else do statin effect besides the syn?

A

statin

good: transcription of LDL receptor, uptake of cholesterol via endocytosis
bad: Myotoxic side effects – depletion of muscle levels of ubiquinone (CoQ 10) - tired, then kills cells

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9
Q

regulators of HMG CoA reductase

A

Direct Inhibition – by free fatty acids, bile acids, oxysterols and statins

Covalent Modification:
low energy, high AMP, activate AMPK, phosphorylates
Insulin - dephosphorylating
Glucagon - phosphorylating it

transcription (mrna), translational (y-tocotrienol, oxylanosterols), post-trans - turnover, degrade enhanced by trans above

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10
Q

is HG CoA reductase active in phospho form or dephospho form

A

active in dephospho form.

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11
Q

what triggers translocation of srebp-scap complex to golgi? high keeps it where

A

low cholesterol

er mem with INSIG (keeps there)

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12
Q

what does srebp do? what does it bind to?

A

Up-regulation of enzymes in cholesterol Biosynthesis and LDL-Receptor (take in cells)

sterol regulatory element (SRE) in its promoter region of nucleus

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13
Q

lipoproteins functions?

A

transport and deliver TAGs , cholesterol homeostasis, targeting signals/ligands, activate various enzymes in lipid metabolism

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14
Q

size and density of lipoproteins

A

hdl, ldl, idl, vldl, chylomicron

order of highest density (small w/ most protein, least tag) to lowest (big w/ least protein, most tag)

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15
Q

Chylomicron markers

A

ApoB-48, ApoC-II, ApoE

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16
Q

VLDL markers

A

ApoB-100, ApoE, ApoC-II

made in liver, w tags and cholesterol

17
Q

markers functions?

A

ApoB-48 - Facilitates transport
ApoE - Facilitates Uptake into liver, uptake into hepatocytes (HDL only)
ApoB-100 - uptake into cells
ApoA-I - Activates enzyme that esterifies cholesterol
ApoC-II - Activates capillary lipoprotein lipase

18
Q

LDL markers

A

ApoB-100

19
Q

HDL markers

A

ApoA-I
ApoC-II
ApoE
high protein and phospholipid content

20
Q

chylomicron processing

A

in SI through lymph to blood
HDL gives ApoC-II and ApoE to mature chylomicron
releases ApoC-II, glycerol and free fatty acids
remnants endocytosed by liver via bind to ApoE receptor

21
Q

what hydrolyzes TAG -> glycerol and free fatty acids from VLPL and chylomicrons? Can cause what disease if there is issues with it?

A

capillary lipoprotein lipase

Type I hyperlipoproteinemia

def in apoc-II (adult)or def lipoprotein lipase(infant), not able to hydrolyze TAGs in chylomicrons and VLDL
increase chlyomicrons and TAGs (>1000 mg/dL)
symp: xanthomas, abd p, acut pancreatitis
low fat diet

22
Q

VLDL, IDL, and LDL Processing

A

vldl in liver to blood
releases ApoC-II to HDL, glycerol and free fatty acids, leaving IDL
ApOE to IDL receptors on liver
IDL
loses more glycerol and free fatty acids, leaving LDL
ApoB-100 to LDL receptors on peripheral tissues

23
Q

What converts TAG -> glycerol and free fatty acids from IDL?

A

tissue lipoprotein lipases and hepatic lipoprotein lipases

24
Q

deficiencies in LDL receptors on peripheral tissue is?

A 
Type IIa (complete)
type IIb (partially defective)

Increase chylomicrons; ldl (both), triacylglycerols and VLDL (IIb only)

25
Q

what is the main carrier of cholesterol

A

LDL, 1500 cholesterol ester mol
apo b-100 recog by recpt in target cells
transport and denovo syn of cholesterol at sites

26
Q

Uptake of LDL:Receptor-mediated Endocytosis

A

endocytoized -> vesicle, -> lysosome, ph breaks down into aa and cholesterol

27
Q

what is it when receptors that are unable to release ldl cargo?

A

familial hypercholesterolemia

normally in endosome, reduced ph converts receptor from open into closed structure, releasing LDL

28
Q

HDL processing

A

disk like HDL in liver, small intestin
gets chol from tissues, LCAT ((lecithin cholesterol acyl transferase) esterifies chol and enters HDL (sphere)
donates apoc-II/ApoE, esters, for tag, phospholipids
delivers to liver

29
Q

what protein facilitates exchanges between HDL and the others?

A

cholesterol ester transfer protein, CETP

30
Q

benefits of HDL

A

maturation of chylomicrons reverse cholesterol transport

HDL scavenges and removes LDL-cholesterol from periphery and transports it to liver where it can be recycled and processed

HDL-C levels increased by weight loss, exercise, and smoking cessation

antioxidant, anti-inflammatory, antithrombotic, and nitric oxide-inducing properties

31
Q

Tangier disease

A

Loss of ABCA1 activity of cholesterol-transport protein

HDL deficiency, accumulation of cholesterol in macrophages, and premature atherosclerosis

ABCA1 binds to ApoA-I apoprotein component of HDL to facilitate transport of LDL

def in transport that supports cholesterol pickup by HDL

32
Q

type II hyperlipoproteinemia

A

defects in LDL receptor resulting in defects inuptake of LDL via Receptor-mediated endocytosis
lots chol in blood
form oxidized LDL -> atherosclerosis
Impaired ability to recognize ApoB 100 on LDL
Xanthomas, corneal deposits in eyes, and angina pectoris

33
Q

levels of cholesterol in T2 Hyperlipoproteinemia

Treatments?

A

Normal cholesterol 130-200 mg/dL
•Heterozygous – 300-500 mg/dL
•Homozygous – >800 mg/dL (die of CAD before teens)

Heterozygous respond to diet, statins and bile acid binding resins
Homozygous need LDL apheresis and liver transplantation

34
Q

Plasma Cholesterol and Atherosclerosis

A

LDL-C in bv -> oxidized LDL (oxLDL) -> build in vessel wall ->endothelial injury and further influx ->Increased vascular permeability and leukocyte adhesion, inflam response ->macrophages engorge to form foam cells -> form plaques-> build up of foam cells, platelet adhesion, and recruitment of smooth muscle cells -> atherosclerosis -> MI

35
Q

IDL markers

A

ApoB-100 and ApoE

CPR I (12 decks)

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