Test 2 - German - Carb Meta Flashcards

1
Q

What is your mnemonic for glycolysis and what do they stand for?

A
Glen - GLU
Grunts - GLU-6-P
Frantically - FRU-6-P
For - FRU-1,6-BP
Dang - DHAP
Good - G3P
Blood - 1,3-BPG
Pressure - 3-PG 
Pressuring - 2-PG
Petty - PEP
Punks - PYR
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2
Q

What is your mnemonic for the allosteric enzymes of glycolysis and what do they stand for?

A
Hungry - Hexokinase
Pirates - Phos-Hex-Iso 
Picked - Phos-Fru-Kinase
All - Aldolase
The - Triose
Greatest - G3PDH
Pickled - PG-Kinase
Pumpkins - PG-Mutase
Ever - Enolase
Picked - Pyr-Kinase
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3
Q

What is the RLS of glycolysis?

A

Fru-6 to 1,6BPFru - catalyzed by phosphofructokinase

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4
Q

What are the necessities and products of glycolysis and where are they generated?

A

1 ATP req’d - Glu to Glu-6
Fru-6 to 16BP

2 NADH made - G3P to 13BPG

2 ATP made - 13BPG to 3PG
PPyr to Pyr

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5
Q

What is the mnemonic for Krebs and what do they stand for?

A
Citrate - Citrate
Is - Isoaconitate
Kreb’s - a-Ketoglutarate
Starting - Succinyl-CoA
Substrate - Succinate
For - Fumarate
Making - Malate
Oxaloacetate - Oxaloacetate
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6
Q

What is the mnemonic for the allosteric enzymes for Kreb’s and what do they stand for?

A
Acorns - Aconitate
|| - ||
Isolate - IsocitDH
Keddington - a-KDHComplex
Sucking - Succinyl-CoA Synthase
Sucky - SuccinateDH
Fumes - Fumarase
MD - MalateDH
Can Say - Citrate Synthase
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7
Q

What is produced from Kreb’s and where in the cycle do they arise?

A

Anywhere there is a DH, an NADH is formed, so Isocit to a-Ketoglu, a-Ketoglu to succinyl-CoA, malate to oxaloacetate.

FADH2 - Formed succinate to fumarate

GTP - Formed from Succinyl-CoA to succinate

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8
Q

What is the RLS of the Kreb’s cycle?

A

Oxaloacetate to Citrate via citrate synthase and availability of acetyl-CoA

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9
Q

Gluconeogenesis is the opposite of glycolysis, except for what extra steps?

A

Pyr to oxaloacetate to PEP
Pyruvate carboxylase
PEP carboxykinase

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10
Q

What electron acceptor must be maintained?

A

NAD+

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11
Q

Where does glycolysis happen?

A

In the cytoplasm

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12
Q

Pentose Phosphate Pathway - What does it do?

A

Produces NADPH - Needed for creating fatty acids and free rad protection. Must be maintained w/in cell

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13
Q

The G3P shuttle happens where?

A

Brain and skeletal muscle

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14
Q

Malate-Aspartate Shuttle happens where?

A

Liver, kidneys, heart

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15
Q

What is apoptosis and what organelle dysfunction is tied to it?

What is necrosis?

A

Cell suicide

Mitochondria

Cell homicide

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16
Q

Why fermentation?

What is the electron acceptor of NADH produced in glycolysis in regards to fermentation?

A

It allows glycolysis to continue by regenerating NAD+.

LACTATE

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17
Q

What are the steps of glycogenesis?

What are the enzymes?

What is the point of regulation?

A
Glu
Glu6P
Glu1P
Uracil DPG
Gly chain
Gly
Hexo
Phos-Glu-Mut
UPD-Glu
Gly Syn *Point of regulation
Gly branching enzyme
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18
Q

The active form of glycogen is phosphorylated or dephosphorylated?

A

Dephosphorylated

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19
Q

What activates glycogenesis?

A

Insulin!

It also activates GLUTs, Hexo, and Gly synthase

20
Q

What activates glycogenolysis?

21
Q

How does glucagon activate glycogenolysis?

A

cAMP activates inactive PKA to active PKA. The glycogen is broken down, phosphorylated, turned to glu-P, and then dephosphorylated to be released from cell (this release of Glu from the cell only happens in hepatocytes)

22
Q

Organism-wide, what intracellular signal regs meta function?

A

ATP/AMP

AMP kinase (AMPK) detects intracellular AMP

*This is important, I guess

23
Q

What turns pyruvate into acetyl-CoA?

A

Pyruvate DH

24
Q

Complex II of the ETC interacts with what step of Kreb’s?

A

Succinate to fumarate, when the FADH2 is created.

25
ETC - Talk me thru it. Complex I
NADH is oxidized to NAD. 4 H+’s pumped into intermembrane space from the matrix and 2 H+’s are loaded onto Q (This reduces ubiquinone to ubiquinol)
26
ETC - Complex II
FADH2 from Krebs moves the Q from II to the QH2 from I.
27
ETC - Complex III
QH2 goes to Cytochrome C after getting 2 pumped H+’s and pumping 4 H+’s into intermembrane space. *Free Rads can be formed here. NADPH helps with that. Thanks Pentose Phosphate Shunt and a healthy diet.
28
ETC - Cytochrome C
T-fers electrons to Complex IV
29
ETC - Complex IV
Electrons loaded onto O2 to form H2O. 2 H+’s pumped into intermembrane space.
30
What happens at the end of the ETC? Where do we get all that ATP?
ATP Synthase. H+s pumped thru to form ATP
31
Where are fatty-acyl CoA’s introduced into the ETC?
Complex II
32
An NADH is worth how many ATP? An FADH2 is worth how many ATP? One Glu molecule produces how much ATP?
2. 5 1. 5 30-32 (Range is due to G3P and Malate Shuttles)
33
What are cofactors?
Inorgo ions Cu, Mg, Zn, Fe
34
Oxidoreductases do what kind of rxns?
REDOX
35
Transferases do what kind of rxns?
Transfers
36
Hydrolases do what kind of rxns?
Hydrolysis
37
Lyases do what kind of rxns?
Cleavages
38
Isomerases do what kind of rxns?
T-fer group to yield isomeric forms
39
Ligases do what kind of rxns?
Formations by condensation coupled to cleavage of ATP
40
What is Km?
Conc. Of substrate at 1/2 max velocity of the enzyme
41
What are the 5 types of inhibition?
``` Irreversible Competitive Uncompetitive Noncompetitive Mixed ```
42
Explain irreversible inhibition.
Perm | Enzyme must be replace
43
Explain comp inhibition.
Inhibitor competes with the substrate
44
Explain uncompetitive inhibition.
Inhibitor binds the ES complex. This slows capacity of rxn and prevents production of product
45
Explain noncomp inhibition.
Inhibitor binds enzyme or ES complex. Substrate binding not affected.
46
Explain mixed inhibition.
Inhibitor binds enzyme or ES complex alone.
47
What happens to Km and Vmax? Comp inhib - Noncomp inhib - Uncomp inhib - Mixed inhib -
Comp inhib - Km moves right, no change in Vmax Noncomp inhib - No change in Km, reduces Vmax Uncomp inhib - Km moves left, reduces Vmax Mixed inhib - Km moves right, reduces Vmax