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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
Q

What 2 things can happen to primary bile salts?

A

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
Q

What are secondary bile salts?

A

Bacteria deconjugate bile salts (remove C7-OH)

27
Q

What are plasma lipoproteins?

A

Spherical macromolecular complexes of lipids and specific proteins (apolipoproteins)
-Aka “big balls of fat”

28
Q

What are the lipoproteins with the lowest density w/ the largest size and highest TAG %?

A

Chylomicrons

29
Q

What are the smallest and densest lipoproteins, w/ the lowest TAG %, also known as “good cholesterol”?

A

HDL

30
Q

What is on the outside of lipoproteins?

A

Amphipathic apolipoproteins, phospholipids (hydrophilic allows it to travel), and nonesterified cholesterol (-OH)

31
Q

What is on the inside of lipoproteins?

A

Neutral lipid core (TAG + cholesteryl esters)

32
Q

What are some functions of apolipoproteins?

A
  • Recognition sites for cell-surface receptors
  • Enzyme activators
  • Structural components
  • Some transferred free between lipoproteins
33
Q

Where are chylomicrons assembled?

A

Only in intestinal mucosal cells

34
Q

What do chylomicrons carry?

A

Dietary (exogenous) TAG, cholesterol, fat-soluble vitamins -> peripheral tissues

35
Q

What is a unique apoprotein to chylomicrons?

A

Apo B48

36
Q

What happens when you just ate fat?

A

Intestinal mucosal cells secrete nascent TAG-rich chylomicrons produced from dietary fat

37
Q

What is transferred from HDL to the nascent chylomicron?

A

Apo C-II and Apo E

38
Q

What is packaged in the mature chylomicron?

A

Apo B-48, Apo C-II, ApoE, TAG, cholesterol, esters

39
Q

What is lipoprotein lipase?

A

Extracellular enzyme on capillaries of adipose tissue, cardiac and skeletal muscle
-Activated by Apo C-II (from HDL) -> degrades TAG in chylomicrons

40
Q

When TAG is degraded what happens to the free fatty acids?

A

Go inside the cells (adipose remakes TAG)

41
Q

When TAG is degraded what happens to the glycerol?

A

Returns to the liver

42
Q

What happens to Apo C-II and Apo E after TAG is degraded?

A
  • Apo C-II is returned to HDL

- Apo E -> chylomicron remnant (facilitates recognition and internalization by the liver)

43
Q

Where are VLDLs produced?

A

In liver from endogenous TAG

44
Q

What is a unique apoprotein to VLDL?

A

Apo B-100

45
Q

What do chylomicrons and VLDLs have in common?

A
  • 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
Q

What happens as VLDLs loses more TAG?

A

Becomes an intermediate (IDL) until becomes LDL

-LDL can go to other tissues and see if any cells need cholesterol

47
Q

What happens to the excess LDL?

A

Binds to specific receptors on extrahepatic tissues and on the liver and are endocytosed

48
Q

What do LDLs contain?

A

Much less TAG and high [cholesterol + cholesteryl esters]

49
Q

What is the primary function of LDLs?

A

Provide cholesterol to peripheral tissues or return it to liver
-NOT to give you a heart attack

50
Q

What will be on the surface of LDL?

A

Apo B-100 and Apo E (from VLDL)

-LDL receptors will recognize these apoproteins -> endocytosis of entire lipoprotein

51
Q

What is the real issue of LDLs?

A

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
Q

What are the good guys that protect you against the ROS?

A

Vitamin E, Ascorbic Acid, Beta-carotene, other antioxidants from diet

53
Q

What happens to chemically modified LDLs?

A

Engulfed by macrophage scavenger receptors

-Not regulated and do not get saturated -> continue to eat until completely engorged w/ modified LDLs -> foam cells

54
Q

What is the beginning of atherosclerosis?

A

Foam cells accumulating and platelets try to aggregate to heal it -> stroke

55
Q

Where are HDLs formed?

A

In blood by addition of lipid to Apo A-1

56
Q

What are some important functions of HDLs?

A
  • 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
Q

What role does LCAT have in reverse cholesterol transport by HDLs?

A

Traps cholesterol inside HDLs by esterification

  • Activated by Apo A-1
  • Secreted by liver
  • Only possible by HDL!!
58
Q

What are the classes of steroid hormones?

A

1) Glucocorticoids (Cortisol)
2) Mineralocorticoids (Aldosterone)
3) Sex hormones (Androgens, estrogens, progestins)

59
Q

Where are steroid hormones synthesized and secreted?

A

Adrenal cortex, ovaries, placenta, testes

60
Q

What are steroid hormones complexed with?

A

Albumin

Biochem Exam 3 (7 decks)

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