fatty acid delivery Flashcards

1
Q

these are diet derived, packaged in the intestine to deliver lipids to various tissues. ApoB-48 is associated.

A

chylomicron

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2
Q

________ activates lipoprotein lipase to release free fatty acids for fuel in adipose tissue, heart and skeletal muscle

A

apoC-II

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3
Q

when fats are depleted, chylomicron remnants go to the liver for absorption via _______ mediated endocytosis

A

apoE

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4
Q

these are packaged in the liver from diet derived and de-novo synthesized lipids. apoB-100 is associated

A

VLDL

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5
Q

__________ take up free fatty acids, and convert them to TAGs for storage

A

adipocytes

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6
Q

______ uses the TAG for energy

A

muscle

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7
Q

these deliver cholesterol to various tissues. for example: muscle and adipose tissue have LDL-receptors and recognize apoB-100 on LDL

A

LDL

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8
Q

these pick up cholesterol from extra-hepatic tissue and returns to liver (reverse cholesterol transport), where it can be metabolized

A

HDL

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9
Q

is a sample of blood plasma that is chylomicron rich more cloudy or more clear?

A

cloudy

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10
Q

________ is anchored to the cell surfaces of several tissues that are exposed to the circulation.

A

LPL - lipoprotein lipase

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11
Q

what specific portion of the cell surface is LPL anchored to?

A

heparin sulfate proteioglycans

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12
Q

what two tissues are the highest levels of expression of LDL found in

A

heart and adipose tissue

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13
Q

does apoC-II activate or inhibit LPL

A

activates

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14
Q

does apoC-III activate or inhibit LPL

A

inhibit

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15
Q

____ hydrolyzes the triglycerides that are carried through the circulation by lipoproteins containing apoB-48 (chylomicrons) and apoB-100 (VLDL)

A

LPL

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16
Q

the hydrolysis of triglycerides on VLDL by LPL leads to the formation of a ________ (smaller/larger) more dense lipoprotein within the circulation

A

smaller

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17
Q

true/false: lipoprotein lipase deficiency is a genetic disorder; causes very low triglyceride levels in circulation and several health complications. fat intake has to be tresitrced to less than 20g/day

A

false - causes very high triglyceride levels

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18
Q

who were the two scientists to discover the LDL receptor pathway?

A

Michael brown and Jospeh goldstein

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19
Q

sit on the outer surface of many types of cells, where they pick up LDLs circulating in the bloodstream and transport them into the cell. Once inside the cell, the LDL is broken down to release cholesterol. The cholesterol is then used by the cell, stored, or removed from the body.

A

LDL receptor

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20
Q

is the process ion removing non-hepatic (extra-hepatic) cholesterol for delivery to the liver, and ultimately for excretion from the body (e.g. cholesterol is used for bile acids/salts synthesis; bile is excreted)

A

reverse cholesterol transport (RCT)

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21
Q

reverse cholesterol transport: RCT requires the transfer of cholesterol and phospholipids from cells to ___________ (almost exclusively proteins; very little lipid) in the circulation - a process called cholesterol efflux

A

nascent HDL

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22
Q

reverse cholesterol transport: is the ability of HDL to scoop up cholesterol particles from plaques in the heart’s blood vessels and move those particles to the liver for disposal.

A

cholesterol efflux

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23
Q

reverse cholesterol transport: nascent HDL is then converted to _______ in the circulation

A

mature HDL

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24
Q

reverse cholesterol transport: mature HDL is then taken up by the _______ (only the lipids and not apoA-I)

25
true or false: only the lipid portion of HDL is taken up by the liver, not ApoA-I. therefore ApoA-I can be reused to form more HDL
true
26
what enzyme is used to convert cholesteryl ester to cholesterol
cholesteryl ester hydrolase
27
this transporter, also known as cholesterol efflux regulatory protein, efluxes lipids to lipid poor ApoA-I
ABCA1
28
what does the conversion of nascent HDL to mature HDL require
enzyme and a transfer protein
29
what enzyme is required for the conversion of nascent HDL to mature HDL
lecithin cholesterol acyl transferase (LCAT)
30
what transfer protein is required for the conversion of nascent HDL to mature HDL
phospholipid transfer protein (PLTP)
31
what enzyme is used to convert cholesterol to cholesteryl ester?
LCAT
32
what is a cofactor for LCAT activity
ApoA-I
33
this transfers excess phospholipids from apoB-100 containing lipoproteins (VLDL, LDL) to HDL.
phospholipid transfer protein
34
what is the importance of phospholipid transfer protein (PLTP)?
- provides phospholipid to expand the HDL surface area - provides lecithin (or phosphatidylcholine) for LCAT activity - contributes to the metabolism of apoB-100 containing lipoproteins (VLDL) into LDL
35
the major receptor responsible for selective uptake of HDL is _________
scavenger receptor class B type I (SR-BI)
36
high dietary ______ increased cholesterol efflux in C57BL/6 mice
n-3 PUFA
37
these act as amphipathic detergents that facilitate the enzymatic digestion and absorption of dietary fats in the intestine they are the principal route by which cholesterol is removed from the body (in the faces)
bile acids/salts
38
where are bile acids/salts formed
liver
39
where are bile acids/salts stored
gall bladder
40
true/false: upon fat intake bile acids/salts are released into the intestine
true
41
__________ is the rate limiting enzyme to convert cholesterol to bile acids
cholesterol 7-alpha hydroxyls (cyp7)
42
what are some steroid hormones derived from cholesterol?
progesterone -> cortisol, corticosterone, testosterone corticosterone -> aldosterone testosterone -> estradiol
43
is the main underlying cause of cardiovascular disease. it is a disease in which plaques build up in the walls of the arteries
atherosclerosis
44
______ LDL cholesterol levels tend to correlate with atherosclerosis.
very high
45
_____ LDL cholesterol levels are negatively associated with heart disease
low
46
this pathogenic form of LDL is formed dye to excess hydrolysis of LDL triglycerides; this occurs when LDL levels are high. this cannot bind to the LDL receptor; it cannot be readily removed from the circulation, thus It is susceptible to chemical modifications (e.g. oxidation
small dense LDL (sd-LDL)
47
this pathogenic form of LDL is the product of the oxidation of LDL protein and lipids.
oxidized LDL (oxLDL)
48
what can prevent oxidation of LDL
dietary antioxidants (vitamin A,C,E)
49
true/false: small density LDL particles are more atherogenic (can form plaques more easily)
true
50
true/false: oxidized LDL is more atherogenic (can form plaques more easily)
true
51
true/false: omega-3 fatty acids increase the amount of small density LDL particles
false! reduce the amount of sdLDL
52
_____ LDL leads to excess lipid deposition and can promote atherosclerosis
high
53
____ LDL reduces lipid deposition and can reduce the progression of atherosclerosis
low
54
____ HDL leads to excess reverse cholesterol transport and can reduce the progression of atherosclerosis
high
55
____ HDL results in less reverse cholesterol transport, thus excess deposited lipids from LDL are not removed
low
56
these lower LDL by removing cholesterol from the liver in the form of bile acids/salts (to prevent the cholesterol from being packaged into VLDL) and by increasing the rate of reverse cholesterol transport e.g. cholestryamine and colestipol
bile acid sequestrants (bile acid/salt binding resins)
57
this lowers LDL by reducing ,over triglyceride synthesis and increasing fat oxidation (reducing VLDL). e.g. fenofibrate, gemfibroizil
fibrates
58
injectable treatment of antibodies that inhibit LDL receptor degradation (via PCSK9). e.g. evolocumab and alirocumab
LDL receptor degradation inhibitors (PCSK9 inhibitors)