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

Cholesterol-Khan Flashcards

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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?
23
Q
  1. What is the rate limiting step of cholesterol synthesis?
Study These Flashcards
A
  1. HMG CoA reductase
24
Q
  1. What are some factors that effect HMG CoA reductase?
Study These Flashcards
A
  1. Insulin (+), glucagon (‐), thyroid hormone (+), cortisol (‐), intracellular HMG CoA
    reductase levels, and intracellular cholesterol levels
25
266. What class of drugs inhibits HMG CoA reductase?
266. Statins
26
267. What receptor regulates cholesterol synthesis and storage?
267. LDL receptor
27
268. What is the function of LXR’s?
268. Put cholesterol in a safer place by transcriptional regulation of key intermediates/enzymes (avoids cholesterol overload)
28
269. What activates LXR’s?
269. Oxysterols
29
270. What do LXR’s heterodimerize with?
270. RXR (retinoid X receptor)
30
271. What do oxysterols indicate?
271. Amount of free cholesterol
31
272. Is NPC1L1 upregulated by LXR’s?
272. No, downregulated (takes less cholesterol up)
32
273. Are CYP7A and ABCG5/ABCG8 upregulated by LXR’s?
273. Yes
33
274. What are some complications of therapeutic LXR activation?
274. Hypertryglyceridimia, enhanced cholesterol esterification and storage, apoptosis and inflammation
34
275. What is the purpose of LXR’s upregulating HDL’s?
275. Return cholesterol from peripheral tissues to liver
35
276. What syndrome is associated with 3‐beta‐delta‐7hydroxylase deficiency?
276. Smith‐lemli‐opitz syndrome
36
277. What are some characteristics of the answer to Smith‐lemli‐opitz syndrome?
277. High plasma 7‐dehydrocholesterol which is toxic, mental retardation and multiple congenital malformations
37
278. How can we treat the answer to Smith‐lemli‐opitz syndrome?
278. Feed cholesterol which can feedback inhibit HMG CoA reductase, or use statins
38
279. In infants what AA is conjugated to bile acids? Adults?
279. Taurine, glycine
39
280. What are the two primary bile acids listed in class?
280. Taurocholic acid, taurchenodeoxycholic acid
40
281. How much bile acids are excreted per day?
281. 0.2‐0.6g/d
41
282. What are the three components that give us a critical micellar concentration?
282. Cholesterol, lecithin, bile salts
42
283. What is the precursor for all steroid hormones?
283. Cholesterol
43
284. Where are glucocorticoids produced ? mineral corticoids? Sex hormones?
284. Zona fasciulata, reticularis; zona glomerulosa; testes and ovary
44
285. What is the most potent gluccocorticoid? What are some of its effects?
285. Cortisol, anti inflammatory, stimulates GNG, sodium retention
45
286. What senses drop in ECFV and causes release of renin?
286. Juxtaglomerular apparatus (JGA)
46
287. Where is testsosterone produced? Estrogen?
287. Leydig cells, ovarian granulose cells
47
288. Does testosterone increase muscle mass?
288. Yes
48
289. What is the main defect in congenital adrenal hyperplasia?
289. 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
290. Describe briefly, vitamin D synthesis
290. 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
291. What are some effects of vitamin D?
291. 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
292. What is the major inducer of 1‐alpha hydroxylase
292. PTH which is induced by low calcium
52
293. What can also stimulate induction of 1‐alpha hydroxylase directly?
293. Hypocalcemia and hypophosphatemia
53
294. What can vitamin D deficiency lead to ?
294. Rickets in children and osteomalacia in adults

5: MBOD Get Pumped haha (7 decks)

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