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Med School > Metabolism 2 > Flashcards

Metabolism 2 Flashcards

0
Q

What particles have ApoB100?

A

VLDL and LDL

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1
Q

What is steatorrhea?

A

Fat in the stool.

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2
Q

What particle(s) have ApoB48?

A

Chylomicrons

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3
Q

What are the three proteins on the surface of chylomicrons? How did they get there?

A

ApoB48: intestinal mucosal cells put it on
ApoCII: HDL puts it on
ApoE: HDL puts it on

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4
Q

What is the fxn of ApoE?

A

Recognized by liver.

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5
Q

What is the fxn of ApoCII?

A

Activates Lipoprotein Lipase which converts TAGs into FAs and moves the FAs into cells. This happens in the blood stream.

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6
Q

After a chylomicron docks to LPL, where does it go, and how has its composition changed?

A

It goes to the liver (ApoE).
Before LPL TAGs > CE.
After LPL TAGs < CE.

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7
Q

What is the rate limiting step in the FA oxidation process?

A

The carnitine shuttle.

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8
Q

How does Acyl-CoA get into the mitochondria?

A
  1. Acyl-CoA > (CATI) > Acyl-Carnitine
  2. Diffuse through outer membrane
  3. Transporter to get into inner membrane
  4. Acyl-Carnitine > (CATII) > Acyl-CoA
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9
Q

What are four things to know about normal beta-oxidation?

A
  1. Four step cycle
  2. 2 carbons cleaved at each step
  3. Acetyl-CoA all go to TCA
  4. NADH, FADH2 go straight to ETC
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10
Q

What is the trick in cis-double bond unsaturated fatty acid oxidation?

A

Turn the cis- into a trans- and then proceed as normal. You lose 1 FADH2.

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11
Q

What is the trick to odd # FA oxidation?

A

Add an extra carbon. Use a coenzyme that uses B12.

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12
Q

VLCFAs- how are they oxidized?

A

In peroxisome. It’s very similar to Mito oxidation, but it produces no FADH2.

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13
Q

Where does Beta-oxidation occur?

A

matrix of mito

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14
Q

What cell types cannot use ketones as fuel?

A

Liver and RBC.

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15
Q

Where are ketone bodies made?

A

Primarily in the liver.

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16
Q

What is the affect/correlation of glucagon and fatty acid synthesis?

A

When glucagon is present, you are not making FAs bc you are burning them.

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17
Q

What is the rate limiting step in FA synthesis?

A

Acetyl-CoA carboxylase (ACC).

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18
Q

How does Acetyl-CoA get out of the mito matrix?

A

It becomes Citrate

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19
Q

What cancer drugs are being explored around citrate?

A

Citrate Lyase: it turns Citrate back into Acetyl-CoA in the cytoplasm. This is important bc Acetyl-CoA in the cytoplasm is used to make FAs, which are needed for lipids in aggressively growing cancers.

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20
Q

What does Acetyl-CoA Carboxylase do?

A

It turns acetyl-CoA into Malonyl-CoA

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21
Q

How does ammonia get from peripheral tissue to the liver? What are the 3 steps?

A
  1. Peripheral Tissues: Glutamate > (add NH4 and ATP) > Glutamine
  2. Liver: Glutamine > (H2O removes NH4) > Glutamate [loss of NH4]
  3. Glutamate > (NADP+ to NADPH) > alpha-Ketoglutarate [loss of NH4]
22
Q

What regulates the urea cycle?

A

N-Acetyl-glutamate. This enzyme regulates Carbamoyl Phosphate Synthetase-1 which is the necessary step for citrulline production.

23
Q

Can Acetyl-CoA make sugar? Why?

A

No. When Acetyl-CoA joins TCA it first joins with OAA. It loses 2 carbons, and then becomes OAA again. The net affect is no gain. OAA can make sugar.

24
Q

What AAs can’t make glucose?

A

Leucine and Lysine

25
Q

What is different about the branch chain amino acids? What are those AAs?

A

Isoleucine, Leucine, Valine.

They are not taken up by portal circulation; they are sensed by the brain an an indicator of nutrient/caloric intake.

26
Q

Phenylalanine makes what AA? Are they both essential?

A

Phenylalanine make tyrosine. Phenylalanine is essential, but tyrosine is not… unless we have no phenylalanine.

27
Q

How does PKU work?

A

Phenylalanine cannot make tyrosine bc of a defect in phenylalanine hydroxylase.

29
Q

What neurotransmitter does tyrosine make?

A

Tyrosine > L-Dopa > Dopamine

*all catecholamines are made from tyrosine

30
Q

Kinase

A

Uses ATP to add phosphates

31
Q

Posphorylase

A

Adds inorganic phosphate without ATP

32
Q

Phosphatase

A

Removes phosphate group

33
Q

Dehydrogenase

A

Catalyzes oxidation-reduction reactions

34
Q

Hydroxylase

A

Adds hydroxyl

35
Q

Carboxylase

A

Transfers CO2 groups with help of biotin

36
Q

What is the rate-determining enzyme for de novo purine synthesis?

A

Glutamine-phosphoribosylpyrophosphate (PRPP) amidotransferase

37
Q

What is the RDE for de novo pyrimidine synthesis?

A

Carbamoyl phosphate synthetase II

38
Q

What is the RDE for the urea cycle?

A

Carbamoyl phosphate synthetase I

39
Q

What is the RDE for fatty acid synthesis?

A

Acetyl-CoA carboxylase

40
Q

How do you treat gout? By what mechanism does this work?

A

Use allopurinol. This inhibits xanthine oxidase, creating a back up of hypoxanthine and xanthine, both of which are more water soluble.

41
Q

What are the 3 C’s that you always confuse? What do they do?

A
  1. Citrate: the way to get carbons out of mito matrix, used for FA synthesis.
  2. Citrulline: in urea cycle, citrulline gets carbons out of the mito matrix. Carbamoyl phosphate is added here, and this is the RDS for the urea cycle.
  3. Carnitine: Acteyl-CoA > Acetyl-Carn > enters mito matrix > Acetyl-CoA. There is a carnitine acyltransferase that puts the carnitine on.
42
Q

What is the RDE for cholesterol synthesis?

A

HMG-CoA

43
Q

What AA does the muscle release, and why?

A

Alanine bc it can carry a N.

44
Q

What enzyme is used for the ping-pong? Which pathway does this go to?

A

PLP. This is used for the urea bc there is the N to get rid of.

45
Q

What AA does muscles always end in?

A

Alanine.

46
Q

What does N-Acetyl-glutamate do?

A

It regulates CPS-1 which starts the urea cycle.

47
Q

What is the function of the salvage pathway in terms of the AA pathway? What is the enzyme that does this?

A

It tries to put a a sugar onto a base, -eg turn AMP into a purine. HGPRT [the lesch-nyman enzyme].

48
Q

Explain the function of SREBP-2.

A

SREBP-2 is the TF that transcribes HMGBT CoA reductase, which is the enzyme used in cholesterol synthesis. It is activated when the cholesterol levels are low.

49
Q

HMG CoA Lyase vs. Reductase, what’s the deal?

A

Lyase: ketone bodies
Reductase: cholesterol

50
Q

What makes heme?

A

porphyrin + Fe2+ = heme

51
Q

Where is heme synthesized?

A
  1. Liver (which produces CP450)

2. Erythrocyte-producing cells of bone marrow

52
Q

What is the committed step in heme synthesis? What activates this? What inhibits this?

A

ALA (delta-aminolevulinic acid).

ALA synthase-1in liver. ALAS-2 in erythroid tissue.

Hemin

53
Q

How are porphyrias inherited?

A

Autosomal dominant.

54
Q

What is the difference between Transerrin, Ferrin, Ferroportin, and Hepcidin?

A
  1. Transferrin: uptake of Fe
  2. Ferrin: sequesters Fe in cells as Fe3+
  3. Ferroportin: efflux of Fe
  4. Hepcidin: secreted from liver when Fe is high to degrade Ferroportin

Med School (24 decks)

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