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5: MBOD Get Pumped haha > Cholesterol-Khan > Flashcards

Cholesterol-Khan Flashcards

1
Q
  1. What is cholesterol a precursor for?
A
  1. Bile acids, steroid formation, vitamin D, etc.
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2
Q
  1. T or F: cholesterol plays a role in artherosclerosis/gallstones.
A
  1. True
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3
Q
  1. What dietary products contain cholesterol listed in lecture?
A
  1. Meat Eggs and Dairy
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4
Q
  1. What is most of cholesterol esterfied to in the circulation?
A
  1. Fatty Acids
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5
Q
  1. What is the majority of cholesterol delivered to the small intestine from ?
A
  1. Biliary cholesterol (800‐1200mg/day)
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6
Q
  1. How much cholesterol is absorbed from the small intestine?
A
  1. 70%
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7
Q
  1. Where are Biliary cholesterol molecules synthesized?
A
  1. Liver
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8
Q
  1. How is circulating cholesterol transported?
A
  1. In lipoproteins with cholesterol on surface and cholesteryl esters in the core
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9
Q
  1. What is the cholesterol transporter of the small intestine?
A
  1. NPC1L1
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10
Q
  1. What helps reflux cholesterol back into the small intestinal lumen and excludes plant
    sterols from entering chylomicrons?
A
  1. ABCG5/ABCG8
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11
Q
  1. What esterfies cholesterol for transport into chylomicrons?
A
  1. ACAT ( Acyl:Cholesterol Acyl Transferase )
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12
Q
  1. What puts cholesterols in chylomicrons?
A
  1. MTP- Puts the cholesterol into the chylomicron particle.
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13
Q
  1. What is the secondary structure of ABCG5/ABCG8?
A
  1. Heterodimer
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14
Q
  1. T or F: ABCG8 and ABCG5 are transcribed in the same direction
A
  1. False
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15
Q
  1. What would a mutation in ABCG8/ABCG5 lead to?
A
  1. Inability to exclude plant sterols
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16
Q
  1. Where is the maximum expression of NPC1L1
A
  1. Proximal jejunum
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17
Q
  1. What drug inhibits NPC1L1?
A
  1. Ezetimibe
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18
Q
  1. What OTC substance can we use to increase dietary sterols and inhibit cholesterol
    absorption thereby lowering plasma cholesterol?
A
  1. Benecol
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19
Q
  1. What is the initial substrate for cholesterol synthesis?
A
  1. Acetyl CoA
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20
Q
  1. Describe briefly, cholesterol synthesis
A
  1. Acetyl coaacetoacetyl CoA via acetyl CoA thiolase3‐hydroxy‐3methylgutaryl CoA
    (HMG CoA) via HMG CoA synthaseMevalonate via HMG CoA reductase (regulatedcommited step) using 2NADPH3 mevalonates form farnesyl pyrophosphate via a series of steps2 farnesyl pyrophosphates joined to make squalene (30 carbon precursor)various decarboxylations etc. to make dcholesterol (27 carbon)
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21
Q
  1. What is the total cost of cholesterol synthesis?
A
  1. 18 moles Acetyl CoA, 36 moles ATP, 16 moles NADPH
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22
Q
  1. How many carbons does cholesterol have?
A
  1. 27
23
Q
  1. What is the rate limiting step of cholesterol synthesis?
A
  1. HMG CoA reductase
24
Q
  1. What are some factors that effect HMG CoA reductase?
A
  1. Insulin (+), glucagon (‐), thyroid hormone (+), cortisol (‐), intracellular HMG CoA
    reductase levels, and intracellular cholesterol levels
25
Q
  1. What class of drugs inhibits HMG CoA reductase?
A
  1. Statins
26
Q
  1. What receptor regulates cholesterol synthesis and storage?
A
  1. LDL receptor
27
Q
  1. What is the function of LXR’s?
A
  1. Put cholesterol in a safer place by transcriptional regulation of key
    intermediates/enzymes (avoids cholesterol overload)
28
Q
  1. What activates LXR’s?
A
  1. Oxysterols
29
Q
  1. What do LXR’s heterodimerize with?
A
  1. RXR (retinoid X receptor)
30
Q
  1. What do oxysterols indicate?
A
  1. Amount of free cholesterol
31
Q
  1. Is NPC1L1 upregulated by LXR’s?
A
  1. No, downregulated (takes less cholesterol up)
32
Q
  1. Are CYP7A and ABCG5/ABCG8 upregulated by LXR’s?
A
  1. Yes
33
Q
  1. What are some complications of therapeutic LXR activation?
A
  1. Hypertryglyceridimia, enhanced cholesterol esterification and storage, apoptosis and
    inflammation
34
Q
  1. What is the purpose of LXR’s upregulating HDL’s?
A
  1. Return cholesterol from peripheral tissues to liver
35
Q
  1. What syndrome is associated with 3‐beta‐delta‐7hydroxylase deficiency?
A
  1. Smith‐lemli‐opitz syndrome
36
Q
  1. What are some characteristics of the answer to Smith‐lemli‐opitz syndrome?
A
  1. High plasma 7‐dehydrocholesterol which is toxic, mental retardation and multiple
    congenital malformations
37
Q
  1. How can we treat the answer to Smith‐lemli‐opitz syndrome?
A
  1. Feed cholesterol which can feedback inhibit HMG CoA reductase, or use statins
38
Q
  1. In infants what AA is conjugated to bile acids? Adults?
A
  1. Taurine, glycine
39
Q
  1. What are the two primary bile acids listed in class?
A
  1. Taurocholic acid, taurchenodeoxycholic acid
40
Q
  1. How much bile acids are excreted per day?
A
  1. 0.2‐0.6g/d
41
Q
  1. What are the three components that give us a critical micellar concentration?
A
  1. Cholesterol, lecithin, bile salts
42
Q
  1. What is the precursor for all steroid hormones?
A
  1. Cholesterol
43
Q
  1. Where are glucocorticoids produced ? mineral corticoids? Sex hormones?
A
  1. Zona fasciulata, reticularis; zona glomerulosa; testes and ovary
44
Q
  1. What is the most potent gluccocorticoid? What are some of its effects?
A
  1. Cortisol, anti inflammatory, stimulates GNG, sodium retention
45
Q
  1. What senses drop in ECFV and causes release of renin?
A
  1. Juxtaglomerular apparatus (JGA)
46
Q
  1. Where is testsosterone produced? Estrogen?
A
  1. Leydig cells, ovarian granulose cells
47
Q
  1. Does testosterone increase muscle mass?
A
  1. Yes
48
Q
  1. What is the main defect in congenital adrenal hyperplasia?
A
  1. 21‐beta‐hydroxylase deficiency (deficiency in mineralcorticoids and glucocorticoids)
    less inhibition of ACTH by cortisol more shunting through pathway and more androgens produced (masculinization of female infants)
49
Q
  1. Describe briefly, vitamin D synthesis
A
  1. Converted to vitamin D3 from 7dehydroxy cholesterol in malpighian layer of skinundergoes hydroxylation at C25 in liver and C1 in kidney to form 1,25 dihydroxycholecaciferol
50
Q
  1. What are some effects of vitamin D?
A
  1. Increased absorption of calcium by transcriptional regulation of enzymes, recruits stem cells to make osteoclasts, absorbs calcium and phosphate more readily in the intestine
51
Q
  1. What is the major inducer of 1‐alpha hydroxylase
A
  1. PTH which is induced by low calcium
52
Q
  1. What can also stimulate induction of 1‐alpha hydroxylase directly?
A
  1. Hypocalcemia and hypophosphatemia
53
Q
  1. What can vitamin D deficiency lead to ?
A
  1. Rickets in children and osteomalacia in adults

5: MBOD Get Pumped haha (7 decks)

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