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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
2 therapeutic approaches to reducing cholesterol absorption
1- add plant sterols like benechol- these will compete with cholesterol for NPC1L1 2- antagonize NPC1L1 with meds like zetia
26
when free fatty acids are added to 2-MAG for triglyceride synthesis, they must be activated. What enzyme is responsible for this activation?
fatty acyl coA synthase
27
what are contained in chylomicrons? (3)
triglycerides phospholipids cholesterol
28
what can be absorbed directly into blood by intestinal capillaries? (3)
small/medium free FA acylglycerols glycerol
29
how are lipids transported in the blood?
lipoproteins (lipid + apolipoprotein)
30
what composes the surface, inner layer and core of lipoproteins?
surface = phospholipids and apoproteins inner layer = free cholesterol core = triglycerides and cholesterol esters
31
largest lipoprotein? smallest?
largest- chylomicron | smallest- HDL
32
most dense? least dense?
most- HDL | least- chylomicron
33
highest lipid/protein ratio? lowest?
highest- chylomicron | lowest- HDL
34
of the 4 subclasses of LDL, which is: largest? most affinity for LPL? most dense? most atherogenic?
largest- LDL I most affinity for LPL- LDL I most dense- LDL IV most atherogenic- LDL IV
35
ApoB48 | assoc with? functions?
assoc with chylomicrons | involved with assembly and exocytosis
36
ApoB100 | assoc with? functions?
assoc with VLDL, IDL, LDL | binds to LDL receptor
37
ApoC-II | assoc with? functions?
assoc with chylomicrons, VLDL, IDL and HDL | activates lipoprotein lipase
38
ApoC-III | assoc with? functions?
assoc with chylomicrons, VLDL, IDL and HDL | activates Lipoprotein lipase
39
ApoE | assoc with? functions?
assoc with chylomicron remnants, VLDL, IDL, HDL | binds LDL receptor
40
ApoA-I | assoc with? functions?
assoc with HDL | activates LCAT
41
what causes congenital abetalipoproteinemia?
lack of ApoB48 synthesis leads to accumulation of triglycerides in enterocytes
42
what protein is involved in chylomicron assembly? functions?
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
describe maturation of chylomicrons in lymph/blood
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
what are the products of the reaction between chylomicrons and LPL? (3)
fatty acids- to muscle/adipose glycerol- to liver, used in gluconeogenesis chylomicron remnants- to liver, degraded
45
familial type III hyperlipoproteinemia
accumulation of chylomicron remnants in plasma caused by lack of ApoE
46
how are chylomicron remnants removed from circulation?
with help of ApoE, chylomicron remnants are taken up by liver and are degraded by lysosomal enzymes
47
action of lipoprotein lipase on triglycerides
removes all 3 FA
48
sites of LPL synthesis (3)
- adipose tissues - muscle (mainly cardiac) - lactating mammary gland
49
ApoC influence of LPL
ApoC-II activates | ApoC-III inhibits
50
2 isoforms of LPL, when is their activity increased
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
what occurs in adipose tissue in the post-absorbative state when insulin/glucagon ratio is low?
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
what is the effect of insulin resistance on lipids?
insulin resistance will decrease stimulation of LPL and lead to increase circulating lipids and increased lipids in liver
53
2 main components of VLDL
- triglycerides (from hepatic resynthesis and de novo from acetly-CoA) - cholesterol (exogenous from chylomicron remnants and endogenous)
54
what Apo is on the surface of VLDL?
ApoB100
55
synthesis of triglycerides in the liver is stimulated by- (2)
excess calories (carbohydrates, alcohol) and high concentrations of fat reaching the liver
56
what facilitates the transfer of lipids to VLDL?
MTTP
57
what changes does VLDL undergo after it is released into circulation?
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
what are the results of the 2 interactions of VLDL with LPL?
VLDL with LPL = IDL + Free FA | IDL with LPL = LDL + free FA
59
2 fates of IDL
- travel back to liver to be degraded by lysosomes | - interact with LPL to form LDL
60
2 fates of LDL
- interact with LDL-R for uptake into cell | - undergo oxidation and then be taken into macrophages to form foam cell
61
what is the major carrier of cholesterol to peripheral tissues?
LDL
62
apoproteins assoc with HDL
ApoA-I (liver, intestine) | ApoA-II (liver only)
63
2 actions of CETP
- gives cholesterol esters to VLDL | - gives triglycerides to HDL
64
3 forms of HDL
- 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
what is the action of hepatic lipase?
acts on HDL2 to hydrolyze/liberate fatty acids and form cholesterol-rich HDL3
66
fate of HDL3
removed from circulation by kidney
67
what ratio of total cholesterol/HDL is a risk for CAD
over 4.5

biochem block 3 (7 decks)

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