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Biochem Exam 3 > Cholesterol, Lipoprotein and Steroid Metabolism > Flashcards

Cholesterol, Lipoprotein and Steroid Metabolism Flashcards

1
Q

What is cholesterol?

A

Steroid alcohol of animal tissues

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2
Q

What are some essential functions of cholesterol?

A
  • Structural membrane component
  • Precursor of bile acids/salts
  • Steroid hormones
  • Vitamin D
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3
Q

What is atherosclerosis caused by?

A

Gradual deposition of cholesterol in endothelial linings of blood vessels -> narrowing of blood vessels
-Increase risk of cardio/cerebro/peripheral vascular disease

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4
Q

What are the 4 major characteristics of the structure of cholesterol?

A

1) Steroid nucleus = 4 fused hydrocarbon rings (A-D)
2) Very hydrophobic, except -OH group at C3 (most plasma cholesterol esterified here to form FA)
3) Hydrocarbon chain attached to C17
4) Single double bond

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5
Q

Where is cholesterol synthesized?

A

In all tissues (liver, intestine, adrenal cortex, ovaries, testes, placenta)

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6
Q

Where do all carbons in cholesterol come from?

A

Acetyl CoA

-Pyruvate by PDH –> Acetyl CoA

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7
Q

What provides the reducing equivalents to make cholesterol?

A

NADPH

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8
Q

Where are the main enzymes required to make cholesterol?

A

Cytosol and smooth ER

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9
Q

What is the rate-limiting, key regulated and irreversible enzyme of cholesterol synthesis?

A

HMG CoA reductase

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10
Q

What does HMG CoA reductase do?

A

Reduces HMG CoA (6-C) -> Mevalonate (6-C)

-Uses 2 NADPH

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11
Q

Where is HMG CoA reductase?

A

Embedded in the ER -> rate-limiting step occurs in the cytosol

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12
Q

What is sterol-dependent gene expression regulation?

A

When low [sterol] -> increased transcription to make more HMG CoA Reductase -> increased production of cholesterol

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13
Q

What is sterol-accelerated enzyme degradation?

A

When high [sterol] -> HMG CoA reductase is degraded

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14
Q

What is sterol-independent phospho/dephosphorylation?

A

AMP-activated protein kinase inactivates HMG CoA reductase

-High [AMP] means low energy, not enough energy to make cholesterol

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15
Q

How is cholesterol synthesis hormonally regulated?

A

Insulin favors upregulation of transcription of HMG CoA reductase

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16
Q

How do the statin drugs work as antihyperlipidemics?

A

Competitively inhibits rate-limiting step in cholesterol biosynthesis (looks like the substrate - HMG CoA)

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17
Q

What is the problem with degradation of cholesterol?

A

Steroid nucleus cannot becomes CO2 and cannot give us energy

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18
Q

What is the only way to eliminate cholesterol?

A

Through the feces; eliminated by conversion to bile acids/salts

  • 95% efficiency
  • Only 5% gets eliminated (this is the way we get rid of the steroid nucleus)
  • Eating more fibers increases the % that gets eliminated
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19
Q

What do bile acids and bile salts do to cholesterol?

A

Add 2-3 -OHs and -COOH to cholesterol

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20
Q

What is the pKa of bile acids/salts?

A

pKa = 6 -> 50/50 protonated/deprotonated in duodenum

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21
Q

Are bile acids/salts polar or non-polar?

A

Amphipathic which makes them emulsifying agents (act as detergents)

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22
Q

What is the rate-limiting enzyme in the synthesis of bile acids?

A

Cholesterol 7-alpha-hydroxylase

-Adds -OH at C7 in cholesterol

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23
Q

What are the 2 main bile acids?

A

Cholic acid and chenodeoxycholic acid

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24
Q

How are bile salts conjugated?

A

Addition of glycine or taurine molecule -> better detergents (increase amphipathic nature)
-Lower pKa -> fully ionized (neg. charged at alkaline pH of bile)

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25
What 2 things can happen to primary bile salts?
1) If you're eating they will be released to the intestine 2) They can be saved in gall bladder for later use - Either way help w/ emulsification of fats
26
What are secondary bile salts?
Bacteria deconjugate bile salts (remove C7-OH)
27
What are plasma lipoproteins?
Spherical macromolecular complexes of lipids and specific proteins (apolipoproteins) -Aka "big balls of fat"
28
What are the lipoproteins with the lowest density w/ the largest size and highest TAG %?
Chylomicrons
29
What are the smallest and densest lipoproteins, w/ the lowest TAG %, also known as "good cholesterol"?
HDL
30
What is on the outside of lipoproteins?
Amphipathic apolipoproteins, phospholipids (hydrophilic allows it to travel), and nonesterified cholesterol (-OH)
31
What is on the inside of lipoproteins?
Neutral lipid core (TAG + cholesteryl esters)
32
What are some functions of apolipoproteins?
- Recognition sites for cell-surface receptors - Enzyme activators - Structural components - Some transferred free between lipoproteins
33
Where are chylomicrons assembled?
Only in intestinal mucosal cells
34
What do chylomicrons carry?
Dietary (exogenous) TAG, cholesterol, fat-soluble vitamins -> peripheral tissues
35
What is a unique apoprotein to chylomicrons?
Apo B48
36
What happens when you just ate fat?
Intestinal mucosal cells secrete nascent TAG-rich chylomicrons produced from dietary fat
37
What is transferred from HDL to the nascent chylomicron?
Apo C-II and Apo E
38
What is packaged in the mature chylomicron?
Apo B-48, Apo C-II, ApoE, TAG, cholesterol, esters
39
What is lipoprotein lipase?
Extracellular enzyme on capillaries of adipose tissue, cardiac and skeletal muscle -Activated by Apo C-II (from HDL) -> degrades TAG in chylomicrons
40
When TAG is degraded what happens to the free fatty acids?
Go inside the cells (adipose remakes TAG)
41
When TAG is degraded what happens to the glycerol?
Returns to the liver
42
What happens to Apo C-II and Apo E after TAG is degraded?
- Apo C-II is returned to HDL | - Apo E -> chylomicron remnant (facilitates recognition and internalization by the liver)
43
Where are VLDLs produced?
In liver from endogenous TAG
44
What is a unique apoprotein to VLDL?
Apo B-100
45
What do chylomicrons and VLDLs have in common?
- Similar destination - Made as a "nascent" lipoprotein and acquire Apo C-II and Apo-E from HDL - Apo C-II activated LPL - LPL degrades TAG
46
What happens as VLDLs loses more TAG?
Becomes an intermediate (IDL) until becomes LDL | -LDL can go to other tissues and see if any cells need cholesterol
47
What happens to the excess LDL?
Binds to specific receptors on extrahepatic tissues and on the liver and are endocytosed
48
What do LDLs contain?
Much less TAG and high [cholesterol + cholesteryl esters]
49
What is the primary function of LDLs?
Provide cholesterol to peripheral tissues or return it to liver -NOT to give you a heart attack
50
What will be on the surface of LDL?
Apo B-100 and Apo E (from VLDL) | -LDL receptors will recognize these apoproteins -> endocytosis of entire lipoprotein
51
What is the real issue of LDLs?
When you have a higher amount of fat then you should the LDLs will be around too long -> exposed to ROS -> chemically modified LDL
52
What are the good guys that protect you against the ROS?
Vitamin E, Ascorbic Acid, Beta-carotene, other antioxidants from diet
53
What happens to chemically modified LDLs?
Engulfed by macrophage scavenger receptors | -Not regulated and do not get saturated -> continue to eat until completely engorged w/ modified LDLs -> foam cells
54
What is the beginning of atherosclerosis?
Foam cells accumulating and platelets try to aggregate to heal it -> stroke
55
Where are HDLs formed?
In blood by addition of lipid to Apo A-1
56
What are some important functions of HDLs?
- Circulating reservoir of APO C-II and E - Reverse cholesterol transport: take up cholesterol FROM peripheral tissues and return it TO liver as cholesteryl esters
57
What role does LCAT have in reverse cholesterol transport by HDLs?
Traps cholesterol inside HDLs by esterification - Activated by Apo A-1 - Secreted by liver - Only possible by HDL!!
58
What are the classes of steroid hormones?
1) Glucocorticoids (Cortisol) 2) Mineralocorticoids (Aldosterone) 3) Sex hormones (Androgens, estrogens, progestins)
59
Where are steroid hormones synthesized and secreted?
Adrenal cortex, ovaries, placenta, testes
60
What are steroid hormones complexed with?
Albumin

Biochem Exam 3 (7 decks)

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