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Biochemistry > Exam 3 November 30 Lecture > Flashcards

Exam 3 November 30 Lecture Flashcards

1
Q

What is an overview of cholesterol?

A
  1. chole- means bile and stereos means solid → found in solid form in gallstones
  2. ubiquitous and essential component of animal cell membranes (about 30% in humans) → controls membrane fluidity (without cholesterol, we die since we can’t make cells)
  3. precursor of bile acids and many steroid hormones
  4. 27 carbons and has an alcohol group
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2
Q

What are the serious implications of cholesterol in human health?

A

atherosclerosis → can lead to coronary artery disease and stroke (higher chance to develop these if you have high cholesterol levels)

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3
Q

What are the sources of cholesterol?

A
  1. diet: 200-300 mg per day

2. de novo synthesis: 1 g per day → produced in virtually all cells but the liver is the major producer

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4
Q

Will eating 1-2 eggs/egg yolks affect your cholesterol levels?

A

will not cause high cholesterol → a good source of cholesterol

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5
Q

What happens if someone has high cholesterol?

A

diet isn’t the only problem since the liver also synthesizes cholesterol (1 g per day) → the body can continually synthesize cholesterol especially if the negative feedback is not working properly

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6
Q

What are the chemical properties of cholesterol?

A
  1. amphipathic molecule → fatty part (hydrophobic part) goes into the membrane
  2. low solubility in water (0.2 mg/ 100 mL)
  3. high concentration in plasma and bile (150-200 mg / 100 mL in plasma of healthy people) → packaged in lipoproteins and transported by lipoproteins as a free form (30%) or cholesterol ester (70%) → (390 mg / 100 mL in bile), solubilized by bile acids and phospholipids → if not solubilized, can precipitate as gallstones
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7
Q

What is cholesterol ester?

A

cholesterol can make an ester bond with a fatty acid (logP is 8) → can go and is stuck to the membrane

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8
Q

What is special about the packaging involving lipoproteins?

A

can increase the solubility of cholesterol which is why there is a high concentration of cholesterol in plasma/blood

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9
Q

How is cholesterol synthesized?

A

synthesized from acetyl CoA in the cytosol

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10
Q

What is the role of HMG-CoA synthase?

A

HMG-CoA in the cytosol is involved in cholesterol synthesis

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11
Q

What is the role of isozyme?

A

isozyme in the mitochondria is involved in ketogenesis → synthesis of ketone bodies occurs in the mitochondria

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12
Q

The cytosol does not have what activity?

A

does not have HMG-CoA lyase activity

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13
Q

What are the two fates of HMG-CoA?

A
  1. in the cytosol: HMG-CoA to mevalonate (by HMG-CoA reductase) → to synthesize cholesterol
  2. in the mitochondria: HMG-CoA to acetoacetate + acetyl CoA (by HMG-CoA lyase)
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14
Q

What is the role of HMG-CoA reductase?

A

to convert HMG-CoA to mevalonate which is an irreversible rate-limiting step (regulation point as well) in cholesterol synthesis

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15
Q

How is HMG-CoA reductase regulated?

A

suppressed by cholesterol (through feedback control)

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16
Q

What do statins target?

A

HMG-CoA reductase

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17
Q

In the reaction to convert HMG-CoA to mevalonate, what does HMG-CoA reductase use?

A

uses NADPH as a reducing cofactor → to generate ATP

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18
Q

What are statins?

A

they are competitive inhibitors for HMG-CoA reductase and are prescribed to lower plasma cholesterol levels (as much as 50%)

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19
Q

What is atorvastatin (Lipitor)?

A

the best selling drug of all time (had an annual sale of $10 billion for years) → became generic in 2012 → is a statin to lower cholesterol since it looks like HMG-CoA

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20
Q

What is the structure of HMG-CoA?

A

has 6 carbons and a COOH group

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21
Q

What is the process from mevalonate to squalene?

A

mevalonate (6 carbons) → isopentenyl pyrophosphate (5 carbons since CO2 is lost and has 2 phosphate groups connected to one another) → geranyl pyrophosphate (10 carbons) → farnesyl pyrophosphate (15 carbons) → squalene (30 carbons)

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22
Q

What is the overall process to get from isopentenyl pyrophosphate to squalene?

A

keep adding more isopentenyl pyrophosphates until squalene (30 carbons) is reached

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23
Q

What is the process of cyclization of squalene?

A

has 4 steps to become cholesterol:
squalene (30 carbons) → squalene 2,3-epoxide (30 carbons, makes an epoxide) → lanosterol (30 carbons) → cholesterol (27 carbons)

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24
Q

What is the main role of cholesterol?

A

to be delivered to cell membranes to maintain their structure

25
Q

What are the fates of cholesterol?

A
  1. stored in the liver as cholesterol ester
  2. sent to other body parts → used as a membrane component and used as a precursor for steroid synthesis
  3. converted to bile acids → primary bile acids, secondary bile acids (produced by microorganisms in the gut), and can be conjugated via an amide bond to either glycine or taurine
26
Q

What is another factor that contributes to high cholesterol levels?

A

humans cannot metabolize cholesterol as an energy source

27
Q

Where are bile acids synthesized?

A

in the liver and stored in the gallbladder

28
Q

What are bile acids?

A

are also called bile salts and have extra hydroxyl groups and a carboxyl group (pKa around 7) → makes bile acids amphipathic

29
Q

What is the fat of bile acids?

A

secreted into the bile → stored in the gallbladder → then secreted into the small intestine

30
Q

What is the main role for bile acids?

A

are emulsifying agents for dietary fat that helps digestion → facilitates hydrolysis by pancreatic lipase and facilitates the absorption of fat soluble vitamins

31
Q

What is the difference between primary and secondary bile acids?

A

primary bile acids are synthesized in the liver (we synthesize them) while secondary bile acids are not synthesized by us in the liver → they are produced by microorganisms in the gut

32
Q

What are some examples of bile acids?

A

cholic acid (primary), deoxycholic acid (secondary), and glycocholic acid (modified amino acid in which glycine is attached to a carboxylic acid group)

33
Q

What is enterohepatic circulation?

A

bring back from the intestine to the liver and then is stored in the gallbladder

34
Q

How much cholesterol is lost per day?

A

250 mg of bile acids and 550 mg of cholesterol are lost per day → which is why we need to make new cholesterol everyday

35
Q

How much bile acids are re-absorbed per day?

A

12-32 g of bile acids are re-absorbed per day

36
Q

What can promote the excretion of bile acids?

A

bile acid sequestrants (such as cholestryramine and colestipol) → patients can take them and more bile acids are lost and helps the liver to overall reduce cholesterol levels (used for patients with high cholesterol levels)

37
Q

What are plasma lipoproteins?

A

complexes of proteins (apolipoproteins) and lipids that form distinct aggregates in plasma and transport lipids from tissue to tissue and participate in lipid metabolism

38
Q

What are the different lipoproteins and how are they distinguished?

A

they are distinguished by their density differences and size differences (density and size are inversely proportional to one another)

39
Q

What is the order of lipoproteins from the HIGHEST to LOWEST density?

A

high density lipoprotein (HDL) → low density lipoprotein (LDL) → intermediate density lipoproteins (IDL) → very low density lipoproteins (VLDL) → chylomicrons

40
Q

What is the order of lipoproteins from LARGEST in size to SMALLEST in size?

A

chylomicrons → very low density lipoproteins (VLDL) → intermediate density lipoproteins (IDL) → low density lipoproteins (LDL) → high density lipoproteins (HDL)

41
Q

What is different about each class of lipoprotein?

A

each class of lipoprotein has a characteristic apolipoprotein composition → apolipoproteins serve as ligands for cell receptors

42
Q

What are the structure of lipoproteins?

A
  1. insoluble core (like an oil drop) → consists of triacylglycerol (yellow) and cholesterol ester (orange)
  2. amphipathic shell that supports the core → is a single layer of phospholipid membrane that consists of phospholipids, cholesterol, and apolipoproteins
43
Q

What is the hydrophobicity of a lipoprotein?

A

outside is hydrophilic and inside is hydrophobic

44
Q

What is the difference between chylomicrons and HDLs?

A

chylomicrons are the largest in size and has lots of triacylglycerol from the diet in its core while HDLs have the least amount of fat and has the highest density

45
Q

What is unique about LDLs?

A

its core contains lots of cholesterol ester which is why it is termed the “bad cholesterol”

46
Q

What is the trend with lipoproteins as they get smaller in size?

A

has a lower fat content which means it also has a higher density

47
Q

What is the role of lipoprotein lipase (LpL)?

A

hydrolyzes triacylglycerol to release glycerol and fatty acids

48
Q

What do HDLs do?

A

are scavengers and travels around the body to collect excess cholesterol back to the liver and cleans up → is termed the “good cholesterol” so high HDL levels are a good thing

49
Q

What is an important function of the liver to check LDL levels?

A

liver brings in LDL to check the levels (feedback loop) to see if it needs to slow down cholesterol synthesis

50
Q

Where are chylomicrons produced and where do they eventually end up?

A

produced in the intestine and are hydrolyzed by LpL into chylomicron remnants which are delivered to the liver or to glycerol and fatty acids that are delivered to peripheral tissues

51
Q

Where are VLDLs produced and where does it eventually end up?

A

VLDLs are produced in the liver and get hydrolyzed by LpL into IDL or glycerol and fatty acids that will go to the peripheral tissues

52
Q

Where are IDLs produced and where does it eventually end up?

A

IDLs are produced from VLDLs and can be hydrolyzed by LpL to LDLs that can go back to the liver or into peripheral tissues or by hydrolyzed to glycerol and fatty acids that will go to the peripheral tissues

53
Q

Where are LDLs produced and where do they eventually end up?

A

LDLs are made from IDLs that get hydrolyzed by LpL and they can go back to the liver or to the peripheral tissues

54
Q

Where are HDLs produced and where do they eventually end up?

A

produced by the liver and end up back at the liver since it collects excess cholesterol to bring back to the liver to clean up

55
Q

What two lipoproteins are produced by the liver?

A

VLDLs and HDLs

56
Q

What happens if there is something wrong in the LDL receptor pathway?

A

the liver does not know and continues to synthesize cholesterol which can then lead to familial hypercholesterolemia

57
Q

What is familial hypercholesterolemia?

A

an inherited genetic condition in which the patient has markedly elevated LDL cholesterol levels beginning at birth due to lack of feedback inhibition in de novo cholesterol synthesis (synthesis can’t be suppressed and liver keeps synthesizing cholesterol) → can lead to premature atherosclerosis and heart attacks

58
Q

What are the causes of familial hypercholesterolemia?

A

mutation in either LDL receptor or apoB100:

  1. little or no LDL receptor production
  2. receptors are synthesized properly but delivered to an improper location on the membrane → like the wrong side of the cell
  3. receptors have impaired binding affinity to LDL → could be due to a mutation in the binding pocket
  4. receptors can bind LDL but cannot be internalized by endocytosis → due to mutation in the endocytosis pathway so that cells cannot bring the cholesterol in to be endocytosed

Biochemistry (18 decks)

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