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MCB II Block 3 > Degradation of dietary lipids > Flashcards

Degradation of dietary lipids Flashcards

1
Q

why are Triacylglycerides the major fat in human diet

A

they are major storage lipid in plants and animals

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2
Q

where does the majority of triacylglyceride digestion take place

A

lumen of intestine

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3
Q

bile salts are what kind of compound

A

amphipathic

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4
Q

secretion of gallbladder and pancreatic enzymes are stimulated by

A

CCK

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5
Q

what happens to dietary fat in SI

A

emulsified by bile salts

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6
Q

what is the major enzyme to digest Triacylglycerides

A

pancreatic lipase

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7
Q

pancreatic lipase is secreted in response to

A

CCK

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8
Q

what is secreted along with pancreatic lipase

A

colipase

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9
Q

how does pancreatic lipase work against Triacylglycerides

A

cleaves ester bonds at each end to create 2 free FA & 2 monoacylglycerol

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10
Q

what is colipase function

A

holds Pancreatic Lipase at interface between lipid & aqueous medium;

  • this causes conformation change in lipase & exposes active site;
  • requires activation by proteolytic chymotrypsin
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11
Q

colipase requires activation via

A

proteolyic chymotrypsin

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12
Q

orlistat is a drug that does what

A

fights obesity by inhibiting gastric & pancreatic lipases

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13
Q

name two pancreatic neutral pH lipid-hydrolases in intestine

A

Cholesterol esterase

Phospholipase A2

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14
Q

what is product after cholesterol esterase acts on choesterol ester

A

cholesterol

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15
Q

what is product after phospholipase A2 acts on phospholipid

A

lysophospholipid

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16
Q

after phospholipase A2 acts on phospholipid, what then removes remaining fatty acyl?

A

lysophospholipase

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17
Q

what is another name for lysophospholipid

A

lysolecithin

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18
Q

what does CCK do

A

gall bladder to release bile
release pancreatic enzymes
slows gatric contractions

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19
Q

what does secretin do

A

promotes release of HCO3-

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20
Q

what does steatorrhea mean

A

lipid malabsorption - fat in stool

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21
Q

TAGs, cholesterol, and phospholipids combine into what

A

chylomicrons (CM)

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22
Q

what happens to LCFA & cholesterol when they are absorbed

A

esterified

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23
Q

how are TAG and cholesterol esters packaged

A

particles of lipid droplet

sourrounded by phospholipids, nonesterified cholesterol, apolipoprotein

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24
Q

are short and medium chain fatty acids esterified

A

no

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25
Q

why aren’t short and medium chain fatty acids esterified

A

they are small enough to enter portal circulation directly, bind to albumin to be brought to liver

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26
Q

what happens once short and medium chain fatty acids enter portal circulation

A

bind to albumin and brought to liver

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27
Q

one albumin can bind how many FFA

A

up to 10

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28
Q

intestinal mucosa assembles and secretes

A

chylomicrons

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29
Q

chylomicrons are the sole

A

lipoprotein carrier of dietary lipid

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30
Q

what is the sole lipoprotein carrier of dietary lipid

A

chylomicron

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31
Q

draw out B-apoprotein gene being transcribed and translated

A

pg 14

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32
Q

in liver the B-apoprotein gene is transcribed into

A

ApoB-110 gene

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33
Q

how many AA in ApoB-110 gene

A

4536

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34
Q

in intestine what happens to B-apoprotein gene

A

RNA editting, creating a stop codon and a smaller product

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35
Q

what editting happens to B-apoprotein gene in intesting

A

C→U (stop codon)

36
Q

what is the resulting protein of intesting modification of B-apoprotein

A

ApoB -48

37
Q

how many AA in ApoB-48

A

2152

38
Q

in ApoB 48 chylomicron assembly with dietary lipid, what else is required

A

MTP

39
Q

what does MTP stand for

A

Microsomal (ER) Triglyceride Transfer Protein.

40
Q

what does MTP do

A

mediates process of Apo48 binding to lipid

41
Q

MTP deficiency causes

A

abetalipoproteinemia. LDM levels low and chylomicrons low. have problem with fat

42
Q

what is the consequence of MTP deficiency

A

lipid deficiency

43
Q

what is abetalipoproteinemia

A

defective assembly of all Apo-B bearing lipoproteins (CM, VLDL, IDL & LDL)

44
Q

what are the two major roles of chylomicron in blood

A

separate fats from H20

signal tissue/cell

45
Q

what does chylomicron signal in blood

A

that a new meal has arrived

46
Q

ApoCII activates

A

LPL & ApoE

47
Q

chylomicrons are emptied out by

A

lipoprotein lipase

48
Q

lipoprotein lipase is indirectly activated by

A

insulin

49
Q

in blood, where is lipoprotein lipase kept?

A

it is held to inner capillary wall

50
Q

what anchors LPL to capillary wall

A

GPI

51
Q

what does GPI stand for

A

glycosylated phosphatidyl-inositol

52
Q

what helps keep LPL in lumen

A

SO4

53
Q

what is “leash” - what connects LPL to GPI to anchor to capillary wall

A

heparan sulfate’s ionizable group

54
Q

if there is LPL deficiency what is observed

A

HUGE amount of fat in blood

55
Q

describe differnet tissue response to LPL

A

different tissues have different Km for LPL to meet the energy needs. Heart and muscle have low Km (so high affinity) b/c they need to obtain FA from LP’s.

56
Q

what are remnants of chylomicron

A

cholesterol ester, phospholipid, Apo B-48 & E, fat-soluble vitamins (esp important); very little TAGs; cholesterol & nitrogenous glycerophospholipids (eg choline, serine) recycled

57
Q

if there is defective chylomicron remnant removal, what is disease

A

type III hyperlipoproteinemia aka familial dysbetalipoproteinemia

58
Q

what bond can we not digest in plants

A

ß 1,4 glycosidic bonds in polysaccharide plant wall

59
Q

we don’t have enzymes to break what bond in plants

A

ß 1,4 glycosidic bond

60
Q

phosphatidylcholine has what kind of bonds

A

ester

61
Q

what does pancreatic lipase do

A

breaks triacylgylcerol into 2 monoacylglycerol

62
Q

bile acids are produced in liver from cholesterol and they are

A

Amphiphobic

63
Q

cholesterol on its own is very

A

hydrophobic

64
Q

acinar cells produce what

A

digestive enzymes

65
Q

pts with cystic fibrosis need to take pill to help

A

digesting food

66
Q

bile acids are derived from

A

cholesterol

67
Q

describe structure of micelle

A

hydrophilic outside hydrophobic component inside

68
Q

if pancreatic lipase is inhibited you inhibit

A

inhibit absorption of fat

69
Q

did orlistat work

A

no.

70
Q

gycerophospholipid

A

component of lipid of bilayer - amphiatic molecule

we get this when we eat animal

71
Q

CCK does what to gastrin

A

stops secretion of gastrin

72
Q

how can you get steatorrhea

A

problems in gall bladder, like stone
gall bladder removed
pancreas not secreting enzymes to lumen of intestine

73
Q

problem with CFTR is what disease

A

cystic fibrosis

74
Q

what causes problem with CFTR

A

deletion which inactivates protein

deletion of one aa causes inactivation of protein b/c it has huge AA

75
Q

on lumen side of cell chloride is exchanged for

A

bicarbonate

76
Q

if you don’t have chloride then what happens in ductal cell (like in cystic fibrosis)

A

don’t have bicarbonate leaving and have problems with pH so digestive enzmes won’t work
problems with water.

77
Q

pts with cystic fibrosis do not have what functional cell

A

acinar

78
Q

pancreatitis

A

digestive enzymes stuck in ducks. the enzymes contain proteases which will digest things. (he said it is another component of cystic fibrosis)

79
Q

ApoB100 is

A

VLDL

80
Q

VLDL

A

very low density lipoprotein

81
Q

when C is deaminated it produces

A

uracil

82
Q

chylomicrons and VLDL contain different proteins but they come

A

from the same gene

83
Q

MTP is internalized in

A

lipid

84
Q

the large ApoB particle will go where for maturation and secretion

A

golgi

85
Q

HDL is

A

cholesterol containing lipoprotein

86
Q

the higher HDL is that good or bad

A

the better it is. related to reduce cardiovascular disease

87
Q

review the concept map at end

A

pg 21

MCB II Block 3 (6 decks)

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