MMT: fuel metabolism I Flashcards

(43 cards)

1
Q

What is the main fuel source in utero?

A

Glucose from maternal circulation

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2
Q

What is the rate limiting enzyme for pyrimidine nucleotide synthesis?

A

Carbamoyl phosphate synthetase II (CPS II)

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3
Q

How much ATP is needed for pyrimidine nucleotide synthesis?

A

5 ATP

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4
Q

What is the rate limiting enzyme for purine synthesis?

A

Glutamine PRPP aminotransferase

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5
Q

How much ATP is needed for purine synthesis?

A

8 ATP

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6
Q

What do we need the pentose phosphate pathway to generate?

A

NADPH and ribose-5-phosphate

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7
Q

What is the rate limiting enzyme for the pentose phosphate pathway?

A

Glucose-6-phosphate dehydrogenase

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8
Q

How do fetal cells generate ATP?

A

Uses glucose from maternal blood received through the placenta as fuel for ATP production

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9
Q

What is the general pathway for ATP production from glucose?

A
  1. Glucose > pyruvate in glycolysis
  2. Pyruvate enters TCA to make NADH, GTP
  3. NADH and NADPH bring protons to power oxidative phosphorylation in which the proton gradient allows ATP synthase to make a bunch of ATP
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10
Q

What happens to maternal response to insulin in the third trimester?

A

Slight insulin resistance; this allows more glucose available for the fetus. There will also be more insulin in the blood due to the resistance

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11
Q

What does the fetus begin to do with glucose in the third trimester?

A

Store it as glycogen and fat

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12
Q

Insulin increases glucose uptake in…

A

Muscle and adipose

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13
Q

Which GLUT is present in muscle and adipose tissue and responds to insulin?

A

GLUT4

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14
Q

Which GLUT is present in the liver and responds to insulin?

A

GLUT2

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15
Q

What are alternate pathways for glucose if it does not enter glycolysis?

A

Pentose phosphate pathway, glycogenesis, fatty acid and cholesterol biosynthesis

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16
Q

What is the general process of glycogen synthesis?

A
  1. Glucose enters the cell and receives a phosphate group
  2. Phosphate group moves from 6 to 1
  3. Glucose-1-phosphate becomes UDP glucose
  4. Glycogen synthase adds glucose to growing glycogen molecule and branching enzymes form structure
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17
Q

What happens as citrate builds up in the mitochondria?

A

It will shuttle into the cytoplasm and convert back to OAA and acetyl CoA. From here, acetyl CoA can become palmitate or cholesterol

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18
Q

Describe the basic process of fatty acid formation from acetyl CoA.

A
  1. Acetyl CoA becomes malonyl CoA via acetyl CoA carboxylase, stimulated by insulin
  2. Fatty acid synthase forms palmitate
19
Q

What does malonyl CoA regulate?

A

It shuts off fatty acid beta oxidation by turning off CPT I! This prevents us from breaking down all the fatty acids we’re trying to make

20
Q

Describe the basic process of cholesterol formation.

A
  1. Acetyl CoA forms HMG CoA
  2. HMG CoA reductase, stimulated by insulin, forms mevalonate
  3. Mevalonate converts to cholesterol
21
Q

What is the most abundant phosphoacylglycerol in our membranes?

22
Q

What is dipalmitoyl phosphatidyl choline?

A

A phosphoacylglycerol that is a key component of surfactant. A lack of it at birth can cause respiratory distress syndrome

23
Q

Describe transport of triacylglycerols from the liver.

A

They leave via VLDL. VLDL will be tagged with apocII, allowing it to interact with LPL at peripheral tissues to release the triglycerides and break them into fatty acid and glycerol. The fatty acids will be taken into the tissue

24
Q

What ligand do LDL receptors use to receive LDL particles?

25
LDL particles do not have which ligands?
ApoE or ApoCII
26
What is a big shift neonates experience at birth in terms of metabolism?
They lose their steady stream of glucose from mom, and must transition to using their livers to buffer blood glucose
27
How does glucagon at birth impact blood glucose and fatty acids?
Causes the liver to break down the glycogen stores that the baby started building in the third trimester. Will also cause the release of free fatty acids via breaking of TGs from adipocytes
28
How does skeletal muscle respond to glucagon?
It doesn’t at all; they don’t have glucagon receptors
29
How does epinephrine impact blood glucose?
Epinephrine causes an increase in cAMP and leads to a phosphorylation cascade that will result in breaking down glycogen
30
How does skeletal muscle respond to epinephrine?
It releases glucose-6-phosphate for use in the tissue! It cannot be used to buffer blood glucose
31
Why can skeletal muscle not buffer blood glucose?
It does not possess glucose-6-phosphatase. As a result, glucose from skeletal muscle cannot be released as free glucose back into the bloodstream and remains as glucose-6-phosphate in the muscle tissue
32
When glycogen phosphorylase is phosphorylated, what happens?
It becomes active and starts to break down glycogen to release glucose
33
When glycogen phosphorylase is dephosphorylated, what happens?
It becomes inactive, allowing for the building of glycogen molecules
34
Why is maintaining glucose homeostasis even harder in a neonate?
They have a larger brain to liver ratio, so they need more glucose for their brain!
35
Who uses more ketone bodies: neonates or adults?
Neonates due to increased brain energy demands
36
How do we get ketone bodies?
b-oxidation of fatty acids
37
What is the purpose of the carnitine shuttle syndrome?
It brings long chain fatty acids into the mitochondria for beta oxidation; small or medium chains may be able to diffuse in by themselves, but longer ones require the carnitine shuttle
38
Describe the carnitine shuttle system.
1. Fatty acids enter the cytoplasm and combine with acetyl CoA 2. CoA is replaced by carnitine via CPT I 3. Acylcarnitine enters the mitochondrial matrix via CACT 4. CPT II exchanges carnitine for a CoA molecule 5. Long chain acyl CoA can undergo beta oxidation
39
What is the rate limiting enzyme of fatty acid oxidation?
CPT I
40
CPT I is inhibited by…
Malonyl CoA
41
What is the rate limiting enzyme for ketone body synthesis?
Mitochondrial HMG CoA synthase
42
What does the cytoplasmic HMG CoA synthase do?
Cholesterol synthesis
43
What does mitochondrial HMG CoA synthase do?
Ketone body synthesis