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BIOL301 > BIOL 301 class 20 > Flashcards

BIOL 301 class 20 Flashcards

1
Q

what is high cholesterol/hyperlipidemia?

A

excessive amounts of lipids in the blood serum

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2
Q

steps of dietary fat processing

A

1) bile salts emulsify dietary fats in the small intestine, forming micelles
2) intestinal lipases degrade triacylglycerols (stored form of fat)
3) fatty acids and other breakdown products are taken up by the intestinal mucosa and converted into triacylglycerols (intestinal mucosa repackages it to triacyglycerols)
4) triacylglycerols are incorporated with cholesterol and apolipoproteins into chylomicrons
5) chylomicrons move through the lymphatic system and bloodstream to tissues
6) lipoprotein lipase, activated by apoC-II in the capillary, converts triacylglycerols to fatty acids and glycerol
7) fatty acids enter cells
8) fatty acids are oxidized as fuel or reesterified for storage

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3
Q

What happens to the intestinal epithelium after having a fatty meal?

A

Fat droplets appear

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4
Q

what are fat droplets?

A

fats that have been absorbed by the intestine and will be repackaged as TAGs into chylomicrons and sent out to the tissues

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5
Q

The lipid and cholesterol circulatory system

A

1) starts at the intestine
- intestine produces chylomicrons
2) chylomicrons go into the capillary
- lipoprotein lipase degrades chylomicrons into free fatty acids which then go to the mammary, muscle, or adipose tissue
3) chylomicron remnants can then go to the liver
4) VLDL remnants (IDL) can also go into the liver
- they can also get degraded to LDLs and go into the liver or extrahepatic tissues
5) HDL precursors (from the liver and intestine) can go into extrahepatic tissues
6) from the extrahepatic tissues these HDLs can also go into the liver via reverse cholesterol transport

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6
Q

what is the big role of the liver during the lipid and cholesterol circulatory system?

A

the liver sends out more proteins to grab more lipids if this is needed via reverse cholesterol transport

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7
Q

what are cholesterol esters?

A

the storage and transported forms of cholesterol

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8
Q

what are the two types of cholesterol esters?

A

ACAT & LCAT

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9
Q

what is ACAT?

A

transfers fatty acids from Fatty AcylCoA to cholesterol in the liver and other cells

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10
Q

what is LCAT?

A

transfers fatty acids from phosphatidylcholine to cholesterol on HDLs during reverse transport

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11
Q

cholesterol is made by?

A

a fatty acid esterifying into a cholesterol molecule

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12
Q

what are serum lipids?

A
  • lipoprotein complexes with different lipid/protein ratios
  • keep it into a soluble form so they dont form a fat globule in the serum
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13
Q

high LDL = ?

A

high cholestrol

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14
Q

high HDL = ?

A

good cholesterol

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15
Q

lipoprotein order from high lipid concentration to low

A

chylomicrons, VLDL, IDL, LDL, HDL

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16
Q

high protein concentration = ?

A

low density

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17
Q

low protein concentration = ?

A

high density

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18
Q

lipoproteins are the delivery vehicles for lipids

A

at the beginning → they have more lipids so they have a lower density
after delivering lipids to peripheral tissues → they are low on lipids so that means they have a higher density

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19
Q

HDLs are vehicles sent to retrieve excess lipids

A

→ reverse transport when needed
→ these proteins are recognized by receptors on cell surfaces
→ these receptors then free up fatty acids for import into the cells that need them.
→ the goal is to ultimately deliver fat for storage and energy purposes

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20
Q

apoliproteins

A

phospholipids, TAGs, and cholesterol circulate in the blood in complexes with apoliproteins

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21
Q

apolipoprotein + lipid = ?

A

lipoprotein

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22
Q

apolipoprotein = ?

A
  • protein alone
  • alpha helix structure
23
Q

lipoprotein structure

A

surface monolayer -> free cholesterol + phospholipids
hydrophobic core -> TAG + cholesterol esters

24
Q

different apoliproteins

A

(A-1, A-II, B, E, etc.) serve as recognition sites for lipoprotein receptors, and/or activators of lipase enzymes

25
Q

chylomicrons are large lipoproteins in apolipoproteins on the surface that serve as recognition sites

A
26
Q

chylomicrons contain

A
  • cholesterol
  • triacylglycerols and cholesteryl esters
  • phospholipids
  • B-48
  • C-III
  • C-II
27
Q

apolipoprotein C-II

A
  • the presence of this protein on the surface of chylomicrons activates lipoprotein lipases in the capillaries which leads to the release of fatty acids and uptake into cells
    -cholesterol, triacylglycerols cholesteryl esters, and phospholipids all start clipping off and being transported into the cell
28
Q

there’s two pathways for lipoproteins and cholesterol transport

A
  • endogenous pathway (lipid homeostasis)
  • Exogenous pathway (dietary)
29
Q

steps of the exogenous pathway

A

1) fatty acids from diet are esterifies to glycerol -> TAGs
- TAGs are packaged into chylomicron lipoproteins and sent out to other tissues
2) capillary lipases are activated by the ApoC-II apolipoprotein, releasing free fatty acids to tissues
3) chylomicron remnants return to the liver where they are taken in via endocytosis

30
Q

endogenous pathway steps

A

1) chylomicron remnants from diet are returned to the liver
2) dietary lipids in excess of need are repackaged in the liver with other apoliproteins to form VLDLs (excess carbs are also converted to fats and repackaged), excess and/or newly synthesized cholesterol is esterified to fatty acids (cholesterol esters) and also packaged as core of VLDLs
3 & 4) VLDLs in the serum deliver free fatty acids and cholesterol via tissues that are in need via activity of lipases
5 & 6) loss of fats from VLDL = LDLs which are returned to the liver and endocytosed by the LDL receptor
7 & 8) HDLs are sent out to the serum to retrieve excess cholesterol and return it to the liver for repackaging or converted to bile salts and stored in the gall bladder

31
Q
  • not all tissues have a receptor for VLDLs (the delivery vehicles) but only the liver has a LDL receptor (the post delivery vehicle) *
A

a form of regulation

32
Q

clearing of LDL from the serum is done via receptor mediated endocytosis

A

1) LDL receptor synthesized in the rough ER and then moved to the plasma membrane via the golgi apparatus
2) LDL receptor binds apoB-100 on LDL, initiating endocytosis
3) LDL is internalized in the endosome
4) LDL receptor is segregated into the vesicle, recycled to the surface
5) endosome with LDL fuses with lysosome
6) lytic enzymes in the lysosome degrades apoB-1oo and cholesterol esters, releasing amino acids, fatty acids, and cholesterol

33
Q

defects in the LDL receptor causes familial hypercholesterolemia

A
  • persistently high levels of cholesterol in the serum which leads to coronary vascular disease
  • the liver is not getting any signal that theres excess fat in the system so its pushing out more fat → more cholesterol in your system
34
Q

defects in cholesterol transport out of lysosome causes lethal nieman-pick type-C disease

A
  • leads to a build up of cholesterol in the liver, spleen and brain
35
Q

cholesterol biosynthesis

A
  • synthesis in the cytoplasm
  • uses cytoplasmic acetyl-coa + NADPH
  • if peripheral cholesterol levels are low, the liver makes more
  • energetically expensive
  • must be highly regulated
  • 3 ATPs needed to make one isoprene precursor, 6 ispoprene precursors needed to make squalene = 18 ATPs needed overall
  • intemediates are also used in synthesis of biologically important molecules and protein modifications
36
Q
  • cholesterol is a precursor for bile salts and steroid hormones *
A
37
Q

bile salts/acids

A
  • amphipathic
  • emulsifying agent
  • only significant mechanism of cholesterol excretion (excess cholesterol can be excreted as bile salts)
38
Q

steroid hormones

A
  • cholesterol-based
  • receptors are transcription factors for things such as progesterone
39
Q

what are oxysterols?

A

oxidized forms of cholesterol that are used to regulate cholesterol synthesis and uptake: probably indicates persistently high levels of cholesterol in the system

40
Q

why does glucagon negatively inhibit cholesterol synthesis?

A
  • glucagon wants to conserve energy and cholesterol synthesis takes up A LOT of energy
41
Q

phosphorylation inactivates HMG-CoA

A
  • insulin stimulates dephosphorylation of PPI, which now cannot inhibit HMG phosphatase
  • HMG phosphatase activates phosphorylated HMG-CoA reductase by removing the phosphate group
42
Q

PPI-1

A

phosphoprotein phosphatase inhibitor - 1

43
Q

what else does AMP kinase inhibit?

A

de novo synthesis of fatty acids (FAs), cholesterol and triglycerides (TGs)

44
Q

what is the commitment step for cholesterol biosynthesis?

A

HMG-CoA reductase
- highly regulated

45
Q

other modes of regulation for HMG-CoA reductase

A

rise in intracellular cholesterol levels also inhibits HMG-CoA reductase activity by inhibiting the enzymes synthesis (transcription) and promoting its degradation

46
Q

statins

A
  • medication used to treat hyperlipidemia
  • reversible competitive inhibitors of HMG-CoA reductase
  • by blocking cholesterol synthesis in the liver cells, it induces an uptake of cholesterol from the blood (reverse cholesterol pathway)
47
Q

hepatic cholesterol

A
  • in the liver
  • reduced hepatic cholesterol synthesis causes a decrease in intracellular cholesterol concentration
  • this stimulates upregulation of LDL receptors and increases the recruitment of LDLs back to the liver
48
Q

serum cholesterol

A
  • apo-A1/HDLs are also sent out and serum cholesterol is decreased by increasing reverse cholesterol transport from the circulation
49
Q

atherosclerosis

A

persistently high levels of serum cholesterol (in LDLs) can cause uncontrolled deposition of cholesterol and fatty acids in skin, muscle, and arteries
- a result of hyperlipidimea

50
Q

atherosclerosis is an inflammatory disease

A

persistent LDLs lead to signals that activate immune cell recruitment and inflammatory responses

51
Q

establishment of foam cells activates inflammatory pathways

A

ROS oxidize LDLs which are scavenged by macrophages; these cells then become “bloated” with fat and become foam cells
- foam cells then send out cytokines that recruit more monocytes → macrophages
- foam cells eventually degrade and die, leaving apoptic bodies and cellular debris

52
Q

reverse cholesterol transport is a target of atherosclerosis therapy

A
  • the HDL apolipoprotein ApoA1 stimulates cholesterol effux from transporters (ABCA1) on macrophage surface
  • packaging as esters by LCAT into maturing HDL particles marks the cholesterol for transport through the serum and back to the liver for removal
53
Q

treating/preventing atherosclerosis by increasing reverse cholesterol transport

A

1) decrease turnover of HDLs
2) decrease transfer of cholesterol to LDLs and VLDLs so HDLs move cholesterol back to the liver for excretion
3) increase amount of cholesterol transporters in macrophages

BIOL301 (15 decks)

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