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BMB 402 > Chapter 16: Lipid Metabolism > Flashcards

Chapter 16: Lipid Metabolism Flashcards

1
Q

What does a high carb diet result in?

A

more lipid biosynthesis

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2
Q

What are the key enzymes involved in fatty acid metabolism?

A

Fatty acyl-CoA synthetase
Carnitine acyltransferase I
Acetyl-CoA carboxylase
Fatty acid synthase

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3
Q

Fatty acyl-CoA synthetase

A

catalyzes priming reaction in fatty acid metabolism

converts free fatty acids in the cytosol into fatty acyl-CoA

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4
Q

Carnitine acyltransferase I

A

catalyzes the rate-limiting step in fatty acid oxidation, linking fatty acyl-CoA molecules to carnitine so they can be transported across the inner mitochondrial membrane

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5
Q

Acetyl-CoA carboxylase

A

catalyzes the rate-limiting step in fatty acid synthesis by forming malonyl-CoA from acetyl-CoA

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6
Q

Fatty acid synthase

A

catalyzes a series of reactions that add C2 units to a growing fatty acid chain

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7
Q

Which enzyme catalyzes the rate-limiting step of fatty acid oxidation?

A

carnitine acyltransferase I

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8
Q

Which enzyme catalyzes the rate-limiting step of fatty acid synthesis?

A

acetyl-CoA carboxylase

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9
Q

What causes fatty acyl-CoA synthetase to differ in specificity?

A

size of the fatty acid

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10
Q

What are the two reactions that fatty acyl-CoA synthetase catalyzes to form fatty acyl-CoA?

A
  • free fatty acid adenylation (ATP coupled)
  • CoA-SH attacks adenylate intermediate and releases AMP
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11
Q

What happens to fatty acyl-CoA if energy cell charge is low?

A

It is imported into the mitochondrial matrix by the carnitine transport cycle.

Fatty acids are then degraded to acetyl-CoA, FADH2, and NADH

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12
Q

What happens to fatty acyl-CoA if energy cell charge is high?

A

fatty acid synthesis is favored

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13
Q

What inhibits mitochondrial transport of fatty acyl-CoA?

A

malonyl-CoA

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14
Q

What controls the carnitine transport cycle?

A

Malonyl-CoA

it inhibits carnitine acyltransferase I and prevents the import of fatty acyl-CoA into the mitochondria

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15
Q

How does the carnitine transport cycle regulate cellular metabolism?

A

Controls the flux of fatty acids to either degrade them (mitochondrial matrix) or synthesize them and membrane lipids (cytosol)

maintains a separate pool of coenzyme A

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16
Q

When are malonyl-CoA levels high?

A

When FA synthesis is occuring (which is why it inhibits transport)

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17
Q

Where does beta oxidation occur?

A

in the mitochondria

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18
Q

What occurs during beta oxidation?

A

fatty acids are degraded 2 C units at a time via thiolysis, generating FADH2, NADH, and acetyl-CoA

consists of four repeatable reactions

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19
Q

What are the steps of beta oxidation?

A
  1. Acyl-CoA dehydrogenase (oxidation)
    - forms FADH2 and trans C=C bond
    - isoform dependent on number of C in FA chain
  2. Enoyl-CoA hydratase (hydration)
    - adds H2O across the C=C bond stereospecifically
  3. 3-hydroxyacyl-CoA dehydrogenase (oxidation)
    - forms NADH
  4. B-ketoacyl-CoA thiolase (thiolysis)
    - forms acetyl-CoA
    - removes C2 unit from the fatty acid
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20
Q

What step of beta oxidation produces FADH?

A

step 1

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21
Q

What step of beta oxidation produces NADH?

A

step 3

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22
Q

What step of beta oxidation produces acetyl-CoA?

A

step 4

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23
Q

How much ATP is yielded from the complete oxidation of palmitoyl-CoA?

A

108 ATP

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24
Q

What is ketogenesis?

A

The process in which excess acetyl-CoA is converted to ketone bodies (acetoacetate and D-beta-hydroxybutyrate)

Occurs during starvation while carbohydrate sources are limited

ketone bodies are exported from the liver into muscle tissues

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25
Q

How many carbons are ketone bodies?

A

4 carbons

26
Q

How can ketone bodies be integrated into the citrate cycle?

A

They can be reconverted back to acetyl-CoA, which enters the citrate cycle

27
Q

Where does fatty acid synthesis occur?

A

in the cytosol

28
Q

What are the components of a triglycerol?

A

glycerol-3-phosphate and 3 fatty acids

29
Q

What is fatty acid degradation dependent on and what is rate-limiting for it?

A

dependent on CoA, FAD, and NAD+

carnitine transport is rate limiting

30
Q

What is fatty acid synthesis dependent on and what is rate-limiting for it?

A

dependent on ACP, NADPH

malonyl-CoA synthesis by acetyl-CoA carboxylase is rate limiting

31
Q

What catalyzes the formation of malonyl-CoA?

A

acetyl-CoA carboxylase adds acetyl-CoA and CO2 to form malonyl-CoA

32
Q

What are elongation enzymes use for?

A

increasing the carbon chain in palmitate to make longer fatty acids

33
Q

What are desaturating enzymes?

A

Membrane bound ER proteins that use oxygen as an oxidant to produce unsaturated fatty acids

34
Q

How are triacylglycerols formed?

A

They are formed from phosphatidic acid.

A dephosphorylation occurs and fatty acids are added through esterification.

35
Q

Where are sphingolipids formed?

A

the endoplasmic reticulum

36
Q

What is the citrate shuttle?

A

A shuttle that gets acetyl Co-A into the cytosol for FA synthesis.

Citrate is exported form the citrate cycle in the mitochondria to the cytosol, where citrate lyase breaks it down to oxaloacetate and acetyl-CoA.

The acetyl-CoA is converted to malonyl-CoA by acetyl-CoA carboxylase. Malonyl-CoA is turned into malonyl-ACP by fatty acid synthase, and then the same enzyme converts this to palmitate.

Oxaloacetate is converted to malate and then pyruvate, and is imported back into the mitochondria where it can reenter the citrate cycle.

37
Q

What allosteric mechanisms modulate acetyl-CoA carboxylase activity?

A

citrate and palmitoyl-CoA

citrate activates the enzyme, palmitoyl-CoA inhibits it

38
Q

What covalent modifications modulate acetyl-CoA carboxylase activity?

A

AMP-activated protein kinase (AMPK) (influenced by glucagon) deactivates the enzyme

39
Q

How does insulin affect AMPK?

A

It promotes inactive AMPK

40
Q

How does AMP affect AMPK?

A

It promotes the active form of AMPK

41
Q

What inhibits carnitine acyltransferase I?

A

malonyl-CoA

42
Q

What inhibits acetyl-CoA carboxylase besides pamitoyl-CoA and AMPK?

A

fatty-acyl CoA

43
Q

Where does cholesterol synthesis primarily occur?

A

in all cells but primarily in the liver

44
Q

What are four main purposes that cholesterol serves in?

A
  1. cell membranes
  2. steroid hormones
  3. bile acids
  4. myelin sheaths
45
Q

What is bile?

A

Bile is made from cholesterol and it helps digest fats by emulsifying them.

46
Q

True or false: cholesterol can be degraded

A

false

47
Q

What is the only way to get rid of cholesterol?

A

convert it to bile

48
Q

What is the rate-limiting step of cholesterol synthesis?

A

the conversion of 3 acetyl-CoA to mevalonate via HMG-CoA reductase

49
Q

How many carbons are in cholesterol?

A

27 carbons

50
Q

What are the three main fates of cholesterol from the liver?

A
  1. can be stored in intracellular lipid droplets
  2. can be packaged into lipoproteins and exported into the circulatory system
  3. can be secreted into the small intestines through the bile duct
51
Q

What form must cholesterol be converted to in order to be stored in lipid droplets?

A

must be converted to a cholesterol ester

52
Q

What drugs can be used to decrease the risk of cholesterol associated cardiovascular disease?

A

statin drugs

53
Q

What are apolipoproteins?

A

Membrane-bound vesicles containing a hydrophobic core and one or more proteins on the surface. They consist of a phospholipid monolayer containing cholesterol and one or more apolipoproteins.

They serve as signaling molecules and depend on the protein to triglyceride ratio

54
Q

Which lipoprotein class has the lowest triglyceride composition?

A

HDL

55
Q

What are some classes of lipoproteins?

A

chylomicrons
VLDL
IDL
chylomicron remnants
LDL
HDL

56
Q

What does HDL do?

A

HDL particles remove cholesterol from the peripheral tissues through apoA-1. Cholesterol from peripheral tissue is taken back into the liver.

The “good” cholesterol

57
Q

What do LDLs do?

A

take cholesterol from the liver and into circulation

the “bad” cholesterol

58
Q

What are SREBPs?

A

Large proteins embedded in the ER membrane that function in cholesterol flux in cells

59
Q

How do SREBPs function in cases on low levels of intracellular cholesterol?

A

Low levels of intracellular cholesterol stimulate binding of SREBPs to SRE sequences in transcriptional control regions of specific genes. This leads to the expression of LDL receptor protein synthesis. These receptors are exported to the cell surface, where they interact with LDL and bring it into the cell.

60
Q

What stage of cholesterol biosynthesis do statins inhibit?

A

Stage 1

61
Q

Where in the cell is cholesterol synthesized?

A

first step in cytoplasm, rest in ER

BMB 402 (14 decks)

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