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biochem block 3 > lipid absorption and lipoproteins > Flashcards

lipid absorption and lipoproteins Flashcards

1
Q

most ingested lipids are in the form of-

A

triglycerides

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2
Q

4 major functions of dietary lipids

A
  • energy source
  • hydrophobic barrier for compartmentalization
  • regulatory/coenzyme
  • homeostasis
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3
Q

lipid digestion usually starts in the ___, exception?

A

usually in the small intestine

exception= infants (lingual and gastric lipases for the lipids in breast milk)

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4
Q

where does emulsification take place? what occurs?

A

in the duodenum, bile salts and peristalsis

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5
Q

where do proteolytic enzymes act in lipids?

A

jejunum

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6
Q

what is the digestion product of triglycerides in the small intestine?

A

2-monoacyglycerol + FA

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7
Q

what is the main enzyme of lipid digestion?

A

pancreatic lipase

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8
Q

describe the functions of bile salts

A

bile salts coat lipid droplets to stop them from re-assocaiting and to make them more accessible to lipases

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9
Q

what type of molecules are bile salts?

A

amphipathic

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10
Q

what type of enzymes are lipase’s?

A

carboxylesterases that act at the lipid water interface

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11
Q

which lipase’s act on exogenous lipids? (5)

A

lingual, stomach, pancreatic, mucosal, some phospholipases

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12
Q

which lipase’s act on endogenous lipids? (4)

A

lipoprotein, hepatic, hormone-sensitive, some phospholipases

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13
Q

how does pancreatic lipase work?

A

removes FA from C3 then C1 to yield 2-monoacylglycerol + FAs

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14
Q

what is a cofactor for pancreatic lipase?

A

colipase- secreted from pancreas and helps by reducing surface tension and anchoring/stabilizing lipase

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15
Q

what enzyme degrades cholesterol esters?

A

pancreatic cholesterol ester hydrolase breaks CE into cholesterol and FA

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16
Q

how are phospholipids digested?

A

1- phospholipase A2 removes FA at C2 = lysophospholipid
2- lysophospholipase removes FA at C1 = glycerylphosphorylbase that can then be excreted or further digested and absorbed

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17
Q

what is the form of lipid when they enter the enterocyte? exit?

A

enter- mixed micelle

exit- chylomicron

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18
Q

3 things contained in mixed micelle?

A

long chain FA
free cholesterol
2-monoacylglycerol

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19
Q

which types of FA do not require micelles for absorption?

A

short and medium chain FA

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20
Q

what happens to bile salts after mixed micelles are absorbed?

A

bile salts remain in the intestine, travel to the ileum where 95% are reabsorbed and sent back to the liver via portal circulation

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21
Q

what enzyme is responsible for the re-formation of triglycerides in the enterocyte? cholesterol esters?

A

DGAT (diglycerol acyltransferase)

ACAT (acyl-CoA cholesterol acyltransferase)

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22
Q

what protein is responsible for import of cholesterol from lumen into enterocyte?

A

NPC1L1

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23
Q

what protein is responsible for export of cholesterol from enterocyte to lumen?

A

ABCG5/G8

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24
Q

cholesterol and non-plant sterols are taken up by the same transporters with similar affinity, why then, is so much less plant sterol absorbed vs. cholesterol?

A

less plant sterol is absorbed because ABCG5/G8 is much more efficient at pumping non-cholesterol sterols back out into the intestinal lumen for excretion

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25
Q

2 therapeutic approaches to reducing cholesterol absorption

A

1- add plant sterols like benechol- these will compete with cholesterol for NPC1L1
2- antagonize NPC1L1 with meds like zetia

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26
Q

when free fatty acids are added to 2-MAG for triglyceride synthesis, they must be activated. What enzyme is responsible for this activation?

A

fatty acyl coA synthase

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27
Q

what are contained in chylomicrons? (3)

A

triglycerides
phospholipids
cholesterol

28
Q

what can be absorbed directly into blood by intestinal capillaries? (3)

A

small/medium free FA
acylglycerols
glycerol

29
Q

how are lipids transported in the blood?

A

lipoproteins (lipid + apolipoprotein)

30
Q

what composes the surface, inner layer and core of lipoproteins?

A

surface = phospholipids and apoproteins
inner layer = free cholesterol
core = triglycerides and cholesterol esters

31
Q

largest lipoprotein? smallest?

A

largest- chylomicron

smallest- HDL

32
Q

most dense? least dense?

A

most- HDL

least- chylomicron

33
Q

highest lipid/protein ratio? lowest?

A

highest- chylomicron

lowest- HDL

34
Q

of the 4 subclasses of LDL, which is: largest? most affinity for LPL? most dense? most atherogenic?

A

largest- LDL I
most affinity for LPL- LDL I
most dense- LDL IV
most atherogenic- LDL IV

35
Q

ApoB48

assoc with? functions?

A

assoc with chylomicrons

involved with assembly and exocytosis

36
Q

ApoB100

assoc with? functions?

A

assoc with VLDL, IDL, LDL

binds to LDL receptor

37
Q

ApoC-II

assoc with? functions?

A

assoc with chylomicrons, VLDL, IDL and HDL

activates lipoprotein lipase

38
Q

ApoC-III

assoc with? functions?

A

assoc with chylomicrons, VLDL, IDL and HDL

activates Lipoprotein lipase

39
Q

ApoE

assoc with? functions?

A

assoc with chylomicron remnants, VLDL, IDL, HDL

binds LDL receptor

40
Q

ApoA-I

assoc with? functions?

A

assoc with HDL

activates LCAT

41
Q

what causes congenital abetalipoproteinemia?

A

lack of ApoB48 synthesis leads to accumulation of triglycerides in enterocytes

42
Q

what protein is involved in chylomicron assembly? functions?

A

Microsomal triglyceride transfer protein (MTTP)

  • adds initial lipid to ApoB48 to form nascent chylomicron
  • adds more triglycerides for maturation
  • also adds lipids to ApoB100 for VLDL synthesis
43
Q

describe maturation of chylomicrons in lymph/blood

A

will acquire ApoC-II and ApoE from HDL
ApoC-II allows activation of LPL
ApoE allows interaction with LDL-R for removal of partially digested chylomicrons from blood

44
Q

what are the products of the reaction between chylomicrons and LPL? (3)

A

fatty acids- to muscle/adipose
glycerol- to liver, used in gluconeogenesis
chylomicron remnants- to liver, degraded

45
Q

familial type III hyperlipoproteinemia

A

accumulation of chylomicron remnants in plasma caused by lack of ApoE

46
Q

how are chylomicron remnants removed from circulation?

A

with help of ApoE, chylomicron remnants are taken up by liver and are degraded by lysosomal enzymes

47
Q

action of lipoprotein lipase on triglycerides

A

removes all 3 FA

48
Q

sites of LPL synthesis (3)

A
  • adipose tissues
  • muscle (mainly cardiac)
  • lactating mammary gland
49
Q

ApoC influence of LPL

A

ApoC-II activates

ApoC-III inhibits

50
Q

2 isoforms of LPL, when is their activity increased

A

muscle/cardiac LPL- low KM, increased activity with exercise (for FA fuel)
adipose LPL- high Km, increased activity in fed state by insulin (for FA storage)

51
Q

what occurs in adipose tissue in the post-absorbative state when insulin/glucagon ratio is low?

A

when insulin/glucagon ratio is low, most FA will be bound to albumin in the blood and used for b-oxidation; difficult to store when glucose levels are low bc there is limited glycerol-3-P

52
Q

what is the effect of insulin resistance on lipids?

A

insulin resistance will decrease stimulation of LPL and lead to increase circulating lipids and increased lipids in liver

53
Q

2 main components of VLDL

A
  • triglycerides (from hepatic resynthesis and de novo from acetly-CoA)
  • cholesterol (exogenous from chylomicron remnants and endogenous)
54
Q

what Apo is on the surface of VLDL?

A

ApoB100

55
Q

synthesis of triglycerides in the liver is stimulated by- (2)

A

excess calories (carbohydrates, alcohol) and high concentrations of fat reaching the liver

56
Q

what facilitates the transfer of lipids to VLDL?

A

MTTP

57
Q

what changes does VLDL undergo after it is released into circulation?

A

1- acquires ApoC-II and ApoE from HDL
2- acquires more cholesterol esters in exchange for triglycerides from HDL via CETP
3- interacts with LPL to liberate FA and form IDL

58
Q

what are the results of the 2 interactions of VLDL with LPL?

A

VLDL with LPL = IDL + Free FA

IDL with LPL = LDL + free FA

59
Q

2 fates of IDL

A
  • travel back to liver to be degraded by lysosomes

- interact with LPL to form LDL

60
Q

2 fates of LDL

A
  • interact with LDL-R for uptake into cell

- undergo oxidation and then be taken into macrophages to form foam cell

61
Q

what is the major carrier of cholesterol to peripheral tissues?

A

LDL

62
Q

apoproteins assoc with HDL

A

ApoA-I (liver, intestine)

ApoA-II (liver only)

63
Q

2 actions of CETP

A
  • gives cholesterol esters to VLDL

- gives triglycerides to HDL

64
Q

3 forms of HDL

A
  • lipid poor pre HDL = ApoA-I, phospholipids
  • nascent(pre-b) HDL = free cholesterol added
  • mature (a) HDL = cholesterol esters from LCAT and exchanges mediated by CETP
65
Q

what is the action of hepatic lipase?

A

acts on HDL2 to hydrolyze/liberate fatty acids and form cholesterol-rich HDL3

66
Q

fate of HDL3

A

removed from circulation by kidney

67
Q

what ratio of total cholesterol/HDL is a risk for CAD

A

over 4.5

biochem block 3 (7 decks)

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