W:3 Biochemistry - Energy producing catabolism Flashcards

1
Q

Where is the direction of the H+ in active transport?

A

Out of the mitochondrial matrix into the intermembrane space

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2
Q

NADH/FADH2 generate more H+, thus more ATP than NADH/FADH2.

A

NADH, FADH2

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3
Q

What is the role of brown and beige fat and how do they process H+ differently than the regular ETC?

A

They generate energy in the form of heat.

They have UCP that dissipates H+ gradient without ATP formation.

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4
Q

What are metabolites that provide energy? (4 energy carriers)

A

ATP, NADH, FADH2, GTP

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5
Q

Where does TCA/Kreb cycle take place?

A

Mitochondria

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6
Q

What and how many high energy products are made in once cycle of the TCA cycle?

A

3 NADH
1 FADH2
1GTP

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7
Q

What is generated in mitochondrial beta oxidation of FA?

A

acetyl-CoA + FADH2 + NADH

Every reaction: FA is 2 carbons shorter

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8
Q

FA is a stable molecule so need to by activated by ____ using ___.

A

Acyl-CoA, ATP

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9
Q

Acyl-CoA is attached to “shuttle” ______ to be transported from _____ to _____.

A

Carnitine, cytoplasm, mitochondria

patients with no carnitine have trouble metabolizing fat; enzymes for beta oxidation are all in mitochondria

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10
Q

Where do FA longer than 22 carbons get preliminary processing?

A

Peroxisomes

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11
Q

Where are ketone bodies made? Degraded?

A

Made in the hepatocytes (liver)

Degraded in mitochondria of cells EXCEPT liver (can’t degrade because they don’t have an enzyme)

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12
Q

What are the three ketone bodies? How many carbons?

A

Acetoacetate
3-Hydroxybutyrate
Acetone
(4 carbons)

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13
Q

What is byproduct of ketone body metabolism (ketoacidosis)? (what you smell in the breath)

A

Acetone (no energy; occurs when there’s too much sugar for prolonged time)

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14
Q

What important metabolites are produced in ketolysis?

A

Acetyl-CoA, NADH

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15
Q

What is generated from conversion of pyruvate –> Acetyl-CoA and where does it happen?

A

NADH, mitochondria

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16
Q

Where does ethanol catabolism occur and what does it generate?

A

Cytosol, mitochondria of hepatocytes; each make 1 NADH (2 total), acetyl-CoA

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17
Q

What enzymes carry out the oxidation reactions?

A

dehydrogenases

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18
Q

Where does glycolysis occur?

A

Cytosol

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19
Q

What are net products of glycolysis?

A

2 ATP (net)
2 NADH
2 Pyruvates

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20
Q

What happens if the mitochondria is not taking up the products of glycolysis? How do you go around it?

A

They will build up, halting glycolysis. Lactic acid metabolism

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21
Q

What process does RBC use to maintain source of ATP?

A

Glycolysis

22
Q

Ketone bodies are made in ___ but catabolized in ___.

A

Liver, cells other than the liver

23
Q

In anaerobic glycolysis, ___ and ___ are consumed and ___ is formed.

A

NADH, pyruvate, lactic acid

24
Q

What is the significance of PPP in cell energy metabolism?

A

Let sugars with other than C-6 enter glycolysis (ribose)

25
Where does PPP take place?
Cytosol
26
What are ways acetyl-CoA can be produced?
Beta-oxidation Ketolysis Decarboxylation of pyruvate Ethanol metabolism
27
RBC lacks mitochondria so they only rely on ____ to produce ATP.
glycolysis
28
Amino acid catabolism: examples of molecules that can enter various cycles are:
Ala --> pyruvate Glu --> alpha KG Two amino groups of Gln --> TCA cycle intermediate
29
Liver makes and breaks down ketone bodies. T/F
F: Liver makes ketone bodies during fasting but hepatocytes don’t catabolize them
30
Erythrocytes lack ___ and have little ___.
Mitochondria, glycogen
31
Glycolysis generates 2, 3-BPG. Why is this significant in erythrocytes?
3-BPG facilitates release of O2 from Hb A (reduces affinity of O2)
32
3-BPG increases/decreases during chronic hypoxia, anemia, or pregnancy
Increases; meaning more O2 release in tissues
33
What glucose transporter does skeletal muscle use? Is this insulin dependent?
GLUT4; yes
34
What is the role of myoglobin in muscle?
Capture the oxygen that hemoglobin released outside the cell; a lot of myoglobin in fibers with a lot of aerobic metabolism
35
What is the function of creatine-phosphate system?
Creating "buffer" that increases pool of readily available ATP Creatine takes P from ATP to generate ADP. The Creatine-P is a ready reserve of ATP. ATP inhibits pathways that create more ATP at equilibrium. Creatine-P "hides" ATP so that the energy building cycles continue
36
What sources of energy do cardiomyocytes use?
EVERYTHING: FA>> glc, ketone bodies, glycerol lactate (to make pyruvate) Make sure metabolism will not exhaust ATP in cell
37
Which tissues use creatine-P?
Skeletal, heart, neurons
38
Are cardiomyocytes insulin dependent?
No; uptake happens with or without insulin
39
The main source of energy for neurons is ______ from ______.
Glucose, blood
40
What glucose transporter do neurons use? Is this insulin dependent?
GLUT1; no, uptake is constant
41
Why is there no FA oxidation in neurons? Two reasons.
1) NADH is more efficient than FADH2 2) FAO may generate ROS Because their mitochondria don't carry a lot of the enzymes for FAO. This is because of efficiency. NADH generates more ATP per O2 compared to FADH2. (not because of diffusion issues with BBB) Neurons don't handle oxygen species as well.
42
Where does PPP take place?
cytosol
43
What pathway generates ribose for nucleotide? What happens when ribose is activated?
PPP (ribose 5-P); | ribose --> PRPP
44
What are the two ways nucleotides are made?
1) De Novo synthesis | 2) Purine Salvage pathway
45
What enzyme is responsible for the purine salvage pathway? What are its two substrates?
HGPRT (hypoxanthine guanine phosphoribosyl transferase); | hypoxanthine, guanine
46
Gout, a _____ disease, is caused by accumulation of _______ in the body (joints) due to protein ______ deficiency in the purine salvage pathway.
X-linked, uric acid, HGPRT
47
What is a possible treatment for gout?
Decrease uric acid by inhibiting xanthine with drug
48
SCID (sever combined immunodeficiency), a _____ _____ disease, is caused by inability to degrade ________ from _______ deficiency.
Autosomal recessive, adenosine, ADA
49
How does ADA deficiency cause SCID?
ADA deficiency means inability to break down adenosine in the body (ADP, ATP). Accumulation means no more synthesis, no new DNA, no lymphocytes (B- cells, T-cells)
50
What is the treatment for SCID?
Gene therapy
51
Skeletal cells: GLUT#, insulin-_____ Neurons: GLUT#, insulin-______ Which cells are insulin independent? (uptake glc constantly without regulation; high demand)
(4, dependent) (1, independent) Neurons and cardiomyocytes (heart)