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PMCOL 344 > Plasma Lipids > Flashcards

Plasma Lipids Flashcards

1
Q

what are some good things that happens if you lower plasma lipids (like cholesterol)

A

reduces incidence of CV disease and associated risks

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2
Q

what are 5 beneficial things about lipids

A
  • stored fuel
  • cell membrane
  • bile acid synthesis
  • steroid hormone synthesis
  • signalling molecules
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3
Q

what is the main precursor for bile acids

A

cholesterol

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4
Q

what are 2 examples of lipid signalling molecules

A

leukotrienes, prostaglandins

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5
Q

what are 4 adverse effects of lipids

A
  • dyslipidemias
  • atherosclresis
  • pancreatitis
  • fatty liver disease
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6
Q

what are the 2 major lipids

A

cholesterol and triglycerides

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7
Q

what kind of structure is cholesterol

A

a sterol

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8
Q

how much of cholesterol is from liver

A

80% is synthesized in the liver

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9
Q

how much of cholesterol is from diet

A

usually 20%

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10
Q

what are triglycerides (structure)

A

ester of glycerol and 3 fatty acids

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11
Q

what is the major dietary fat

A

triglycerides

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12
Q

how are triglycerides synthesized in the body

A

in the liver from free fatty acids or excess carbs in the diet

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13
Q

how is triglycerides stored

A

in adipose tissues

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14
Q

what is dyslipedemia

A

alterations in levels of lipids in the blood

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15
Q

what is hypercholesterolemia

A

high cholesterol levels in the blood

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16
Q

what is hypertriglyceridemia

A

high TG levels in the blood

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17
Q

what is hyperlipoproteinemia

A

high LDL or VLDL

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18
Q

what are 4 types of dyslipidemia

A

hypercholesterolemia, hypertriglyceridemia, hyperlipoproteinemia, low HDL

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19
Q

what do LDL and VLDL do (generally)

A

transport mechanisms in the blood stream, bind to parts of body and release cholesterol and TG where needed

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20
Q

how are plasma lipids transported

A

transported in large molecules (lipoproteins), aids solubility in aqueous plasma

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21
Q

what is the structure of plasma lipids like

A

central core of hydrophobic lipid (cholesteryl esters)

hydrophilic coat of free cholesterol, phospholipids and apoproteins

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22
Q

what are apoproteins

A

stabilize particles, function as ligands for lipoprotein uptake - regulate lipoprotein metabolism

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23
Q

where are plasma lipids assembled

A

in the liver

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24
Q

what are chylomicrons + what do they do

A

plasma lipoprotein that transports dietary TGs and cholesterol absorbed from GI tract to tissues

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25
what is the largest plasma lipoproteins
chylomicrons
26
when are chylomicrons present
3-6 hours after meals
27
what does lipoprotein lipase do
releases free fatty acids and glycerol from TGs to leave CM remnant
28
what are CM remnants +where do they go
largely cholesterol, taken up by liver
29
how are CM remnants taken up by liver
via a receptor recognizing apoE
30
what happens once chylomicrons goes to a cell
lipoprotein lipase releases free fatty acids and glycerol from TGs to leave CM remnant
31
what doe VLDL stand for
very low density lipoproteins
32
where are VLDL
made in liver
33
what is the half life of VLDL
less than 30 mins
34
what do VLDL do
transport TGs and cholesterol to tissues
35
what happens once VLDL gets to cells
TGs are hydrolyzed by lipoprotein lipase to release free fatty acids and glycerol, leaves LDL and IDL (intermediate)
36
what does LDL do
deliver cholesterol to the body
37
what is the half life of LDL
1-2 days
38
what is LDL made up of
largely cholesterols (2/3 of plasma cholesterol)
39
how is LDL taken up by tissues and liver
via apoB-100 receptors (LDL receptor)
40
what is the most effective way to reduce plasma cholesterol
increasing hepatic LDL receptor expression
41
why is increasing hepatic LDL receptor expression the most effective way to reduce plasma cholesterol (example)
by reducing dietary cholesterol, inhibiting hepatic cholesterol synthesis
42
what regulates LDL receptor expression
sterol regulatory element binding proteins
43
what does LDL receptor mutations cause
hypercholesterolemia
44
what do sterol regulatory element binding proteins (SREBPs) do
regulates LDL receptor expression
45
what is lipoproteina (Lp(a))
subset of LDL which in addition to apoB-100 also has apo(a)
46
how is apo(a) attached to apoB-100 in lipoproteina
disulfide bond
47
where is lipoproteina often found
localized in plaques
48
what is the structure of apo(a) like (what does this cause)
related to plasminogen, interferes with fibrinolysis on plaque surface (pro thrombotic)
49
what might lipoproteina make a link between
cholesterol and thrombosis
50
is lipoproteina pro or anti atherogenic
pro
51
is apo(a) pro or anti thrombotic
pro
52
what happens to plaque breakdown if Apo(a) is on the surface
prevent breakdown of plaques
53
what might provide the link between cholesterol and thrombosis
lipoproteina
54
what is apoB-100 receptor
LDL receptor
55
what is apoE
part of chylomicron remnants, a receptor in the liver recognizes it and takes it up
56
What is the main role of HDL
remove cholesterol from tissues (reverse cholesterol transport)
57
where is HDL made
in the liver
58
what is HLD made of
mostly phospholipids and apo A1
59
what does HLD to with VLDL and LDL
they can transfer cholesterols to vlDZL and LDL
60
how is free cholesterol from cells transported to HDL
via ABCA1 membrane transporters
61
what is ABCA1
membrane transporter that facilitates transport of free cholesterol from cells to HDL
62
what happens if you have an ABCA1 mutation
low plasma HDL and cholesterol accumulation in tissues
63
what is lecithin cholesterol acyltransferase (LCAT)
it esterifies free cholesterol and moves it to the core of HDL
64
what is cholesteryl ester transfer protein (CETP)
it transfers cholesterol from HDL to VLDL and LDL
65
where is Apo A1 found
in high levels in HDL
66
where does apo a1 bind
with phospholipids on non HDL particles
67
how is cholesterol esterified before moving into the core of HDL
lecithin cholesterol acyltransferase (LCAT)
68
what transfers cholesterol from HDL to VLDL and LDL
cholesteryl ester transfer protein (CETP)
69
how is HDL taken up by the liver
with an HDL receptor that recognized apo A1
70
how does the liver recognize HDL so it can take it up
it recognizes apo A1
71
what happens if you have Apo A1 mutations
reduced HDL uptake, accelerated atherosclerosis
72
which lipid particle is associated with apo A1
HDL
73
which lipid particle is associated with apo(a) and apoB-100
Lipoprotein a (subset of LDL)
74
which lipid particle is associated with apoB-100
LDL
75
which lipid particle is associated with apoE
chylomicron remnants
76
how is plasma HDL level and risk for coronary heart disease
inversely
77
what may be the strongest predictor of coronary heart disease related events
low levels of HDL
78
what a re 4 benefits of HDL other than lipid stuff
anti: inflammatory, coaguland, oxidant and aggregatory
79
what is the role of liver cholesterol levels
it acts as feedback mechanism to regulate further synthesis and uptake
80
what does high liver cholesterol levels cause
decreased synthesis and inhibit LDL receptor expression
81
what happens if the liver reduces LDL receptor expression (like when you have high liver cholesterol levels)
it means that you will reduce uptake, which then causes elevated circulating LDL
82
what is the mechanism to get rid of cholesterol in liver
bile production
83
how many mechanisms are there to get rid of cholesterol in liver
1- bile production
84
how is bile produced
cholesterol is oxidized to bile acids or excreted in bile
85
what is a critical gateway for regulation of plasma cholesterol levels
the liver
86
how much % of bile acids is reabsorbed further down the GI tract
more than 95%
87
what happens if you interrupt bile acid reabsorption
it is effective in increasing hepatic bile synthesis
88
how does increasing hepatic bile synthesis help you? + 1 bad thing
it depletes hepatic cholesterol, then increases LDL receptor expression, so more LDL uptake but then it may also increase hepatic cholesterol synthesis

PMCOL 344 (27 decks)

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