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metabolism 3206 > fatty acid delivery > Flashcards

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)

A

liver

25
Q

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

A

true

26
Q

what enzyme is used to convert cholesteryl ester to cholesterol

A

cholesteryl ester hydrolase

27
Q

this transporter, also known as cholesterol efflux regulatory protein, efluxes lipids to lipid poor ApoA-I

A

ABCA1

28
Q

what does the conversion of nascent HDL to mature HDL require

A

enzyme and a transfer protein

29
Q

what enzyme is required for the conversion of nascent HDL to mature HDL

A

lecithin cholesterol acyl transferase (LCAT)

30
Q

what transfer protein is required for the conversion of nascent HDL to mature HDL

A

phospholipid transfer protein (PLTP)

31
Q

what enzyme is used to convert cholesterol to cholesteryl ester?

A

LCAT

32
Q

what is a cofactor for LCAT activity

A

ApoA-I

33
Q

this transfers excess phospholipids from apoB-100 containing lipoproteins (VLDL, LDL) to HDL.

A

phospholipid transfer protein

34
Q

what is the importance of phospholipid transfer protein (PLTP)?

A
  • 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
Q

the major receptor responsible for selective uptake of HDL is _________

A

scavenger receptor class B type I (SR-BI)

36
Q

high dietary ______ increased cholesterol efflux in C57BL/6 mice

A

n-3 PUFA

37
Q

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)

A

bile acids/salts

38
Q

where are bile acids/salts formed

A

liver

39
Q

where are bile acids/salts stored

A

gall bladder

40
Q

true/false: upon fat intake bile acids/salts are released into the intestine

A

true

41
Q

__________ is the rate limiting enzyme to convert cholesterol to bile acids

A

cholesterol 7-alpha hydroxyls (cyp7)

42
Q

what are some steroid hormones derived from cholesterol?

A

progesterone -> cortisol, corticosterone, testosterone

corticosterone -> aldosterone

testosterone -> estradiol

43
Q

is the main underlying cause of cardiovascular disease. it is a disease in which plaques build up in the walls of the arteries

A

atherosclerosis

44
Q

______ LDL cholesterol levels tend to correlate with atherosclerosis.

A

very high

45
Q

_____ LDL cholesterol levels are negatively associated with heart disease

A

low

46
Q

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

A

small dense LDL (sd-LDL)

47
Q

this pathogenic form of LDL is the product of the oxidation of LDL protein and lipids.

A

oxidized LDL (oxLDL)

48
Q

what can prevent oxidation of LDL

A

dietary antioxidants (vitamin A,C,E)

49
Q

true/false: small density LDL particles are more atherogenic (can form plaques more easily)

A

true

50
Q

true/false: oxidized LDL is more atherogenic (can form plaques more easily)

A

true

51
Q

true/false: omega-3 fatty acids increase the amount of small density LDL particles

A

false! reduce the amount of sdLDL

52
Q

_____ LDL leads to excess lipid deposition and can promote atherosclerosis

A

high

53
Q

____ LDL reduces lipid deposition and can reduce the progression of atherosclerosis

A

low

54
Q

____ HDL leads to excess reverse cholesterol transport and can reduce the progression of atherosclerosis

A

high

55
Q

____ HDL results in less reverse cholesterol transport, thus excess deposited lipids from LDL are not removed

A

low

56
Q

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

A

bile acid sequestrants (bile acid/salt binding resins)

57
Q

this lowers LDL by reducing ,over triglyceride synthesis and increasing fat oxidation (reducing VLDL). e.g. fenofibrate, gemfibroizil

A

fibrates

58
Q

injectable treatment of antibodies that inhibit LDL receptor degradation (via PCSK9). e.g. evolocumab and alirocumab

A

LDL receptor degradation inhibitors (PCSK9 inhibitors)

metabolism 3206 (7 decks)

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