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BIOCHEM 411 w/ Park > EXAM 1 > Flashcards

EXAM 1 Flashcards

1
Q

AT 37℃≈ …?

ΔG°’ ➙ [B]/[A]

A

37℃≈ -6log Keq

ΔG°’ [B]/[A]
0 1
-6 10
-12 100
6 0.1
12 0.01

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2
Q

name the energy compounds that are substantially higher energy than ATP vs roughly comparable

A

higher energy:

✩ Phosphoenolpyruvate (PEP)
✩ 1,3-Bisphosphoglycerate (1,3 BPG)

roughly comparable to ATP:

✫Phosphocreatine (P-creatine)
✫ Thioester bonds ( ex. in Acetyl-CoA)
✫ UDP-Gluc
✬ other NTP

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3
Q

List the most oxidized to most reduced form of carbon

A
  • Carboxylic Acid
  • Aldehyde ( or Ketone)
  • Alcohol (Alkene)
  • Alkane
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4
Q

Draw structure of ATP

A

Slide 24 of lecture 1

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5
Q

Draw structure of 1,3 BPG

A

slide 28 of lec 1

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6
Q

Draw PEP —> Pyruvate

A

slide 27 of lec 1

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7
Q

Acetyl CoA contains___, which is a ____

A

Pantothenic acid, vitamin

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8
Q

What vitamin is found in the nicotinamide part of NADH and what is the deficiency of it called?

A

Niacin; Pellegra

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9
Q

Draw the structure of NAD+ and NADH?

A

Slide 46 of lec. 1

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10
Q

What vitamin is FADH2 made out of?

A

Riboflavin

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11
Q

Which steps in glycolysis are irreversible and serve as regulatory points?

A

✪ hexokinase (step 1)
✪phosphofructokinase-1 (step 3)
✪pyruvate kinase (step 10).

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12
Q

T/F glycolysis occurs in the mitochondria

A

FALSE. It occurs in the cytoplasm of the cell.

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13
Q

What is the first step of glycolysis?

A

the phosphorylation of glucose to form glucose-6-phosphate, catalyzed by the enzyme hexokinase.

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14
Q

Which enzyme is responsible for converting glucose-6-phosphate into fructose-6-phosphate?

A

The enzyme phosphoglucose isomerase

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15
Q

What is the role of phosphofructokinase-1 (PFK-1) in glycolysis?

A

PFK-1 is a key regulatory enzyme in glycolysis that catalyzes the phosphorylation of fructose-6-phosphate to fructose-1,6-bisphosphate

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16
Q

What are the end products of glycolysis?

A

2 molecules of pyruvate, 2 molecules of NADH, and a net gain of 2 ATP molecules.

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17
Q

How does glycolysis contribute to anaerobic respiration?

A

In anaerobic conditions, pyruvate produced from glycolysis can be converted into lactate (in animals) or ethanol (in yeast) to regenerate NAD+, allowing glycolysis to continue producing ATP.

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18
Q

What is the fate of pyruvate after glycolysis under aerobic conditions?

A

Under aerobic conditions, pyruvate is transported into the mitochondria and converted into acetyl-CoA, which enters the citric acid cycle (Krebs cycle) for further energy production.

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19
Q

What happens in the fourth step of glycolysis, and which enzyme is responsible?

also state which one is a ketose and which one is an aldehyde

A

fructose-1,6-bisphosphate is cleaved into two three-carbon molecules: glyceraldehyde-3-phosphate (GAP)
(aldehyde)
and dihydroxyacetone phosphate (DHAP). (ketose)

The enzyme responsible is aldolase (*and Triose phosphate Isomerase)

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20
Q

T/F aldolase alone converts fructose-1,6-bisphosphate to GAP + DHAP

A

FALSE; it needs Triose Phosphate Isomerase as well

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21
Q

Describe the fifth step of glycolysis and the enzyme involved.

A

conversion of dihydroxyacetone phosphate (DHAP) into glyceraldehyde-3-phosphate (GAP).

The enzyme involved is triose phosphate isomerase. (it has to catch up :0 )

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22
Q

T/F every reaction of glycolysis requires Oxygen

A

FALSE; none of the reactions require O2

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23
Q

T/F Taking large amounts of vitamin B1 can enhance athletic performance by stimulating pyruvate decarboxylase and thus reducing feedback inhibition of pyruvate kinase.

A

FALSE; PYRUVATE DECARBOXYLASE DOES NOT OCCUR IN THE LIVER!!!

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24
Q

T/F Hexokinase is the primary enzyme in liver that converts glucose to glucose-6-P

A

FALSE; Hexokinase does NOT occur in the liver, that is GLUCOKINASE

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25
Q

What is the sixth step of glycolysis, and which enzyme catalyzes the reaction?

A

oxidation of GAP to 1,3-bisphosphoglycerate.

This step is catalyzed by glyceraldehyde-3-phosphate dehydrogenase and involves the reduction of NAD+ to NADH

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26
Q

What occurs during the seventh step of glycolysis, and what enzyme is responsible?

A

1,3-bisphosphoglycerate is converted into 3-phosphoglycerate.

The enzyme phosphoglycerate kinase catalyzes this reaction, which generates ATP from ADP.

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27
Q

What enzyme catalyzes the eighth step of glycolysis, and what is the product?

A

The eighth step involves the conversion of 3-phosphoglycerate to 2-phosphoglycerate.

The enzyme responsible is phosphoglycerate mutase.

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28
Q

Describe the ninth step of glycolysis and the enzyme involved.

A

The ninth step is the dehydration of 2-phosphoglycerate to phosphoenolpyruvate (PEP).
The enzyme involved is enolase

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29
Q

What is the final step of glycolysis, and which enzyme catalyzes it?

A

conversion of phosphoenolpyruvate (PEP) to pyruvate. This step is catalyzed by pyruvate kinase and results in the production of ATP.

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30
Q

Compare Hexokinase vs Glucokinase in terms of: usage, location, Km, capacity, mechanism, and how much glucose it takes

A

usage
Hexokinase: Gluc. Fruct. or Mannose
Glucokinase: Glucose ONLY

location
Hex: typical cell
Gluc: Liver

Km
Hex: 0.1 mM
Gluc: 10 mM
portal vein: 5 mM

capacity
Hex: Low capacity
Gluc: High capacity

mechanism
Hex: Direct feedback regulation by G6P
Gluc: Diff. regulatory mechanism (after G6P goes to glycogen n fat)

how much?
Hex: v. polite! takes only as much glucose as needed
Gluc: Stores excess gluc, but doesn’t compete w/ other tissues

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31
Q

What carbons from Fructose-1,6-bisphosphate turn into DHAP and GAP

A

C4=C3
C5=C2
C6=C1

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32
Q

Why is pyruvate kinase named that way?

A

Even though it is irreversible (in vivo), it can still go the opposite direction ONLY in vitro. So it is the enzyme named for reverse reaction (that doesn’t occur in living cells)

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33
Q

Lactate Dehydrogenase

A

reduces pyruvate to lactate using NADH
-reversible

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34
Q

Hexokinase/Glucokinase (allosteric regulation)

A

✮ Glucose 6 phosphate inhibits Hexo
✬ Fructose 6 phosphate inhibits Gluco

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35
Q

Phosphofructokinase-1 (PFK-1) (allosteric regulation)

A

Activated by:
❁AMP: Signals low energy status, promoting glycolysis.
❁Fructose-2,6-bisphosphate

Inhibited by:
❁ATP: Indicates high energy status, slowing down glycolysis.
❁Citrate: Reflects a high level of TCA cycle intermediates, reducing glycolysis. (found in mitochondria!!)

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36
Q

Pyruvate Kinase (allosteric regulation)

A

Activated by:
✪Fructose-1,6-bisphosphate
✪ AMP

Inhibited by:
✪ATP: Indicates sufficient energy levels.
✪Alanine: A building block for protein synthesis, suggesting that resources should be diverted from glycolysis.

✪ Acetyl-CoA

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37
Q

Aerobic vs Anaerobic Glucose Metabolism

A

Aerobic
Gluc–> 6 CO2
ATP gluc ≈ 38
Max flux: 1
Max Energy Output: 38

Anaerobic
Gluc–> 2 lactate
ATP gluc = 2
Max flux: 100
Max energy Output: 200

** ≈3 ATP/ Gluc if starting from Glycogen

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38
Q

What is going on in your muscles vs liver when you’re running for your life?

A

Muscles (can be anaerobic): Is doing Glycolysis
☞Glycogen➙ Gluc (➙G6P) ➙ Pyruvate ➙Lactate

Liver (Aerobic): is doing Gluconeogenesis
☞ Lactate ➙ Pyruvate➙ Gluc ➙Glycogen
(liver then pulls lactic acid levels down)

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39
Q

When running for life, an enzyme like PFK1 would be turned on or off in muscles/ liver?

A

muscles: ON
liver: OFF (don’t want to do glycolysis)

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40
Q

Draw lactate fermentation mechanism

A

slide 53 of lec 2

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41
Q

What is the disease name of TPP deficiency? Name the vitamin and the people who get it

A

*BeriBeri
*Vitamin B1
*People who eat only white rice and alcoholics

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42
Q

Draw the Thiazolium ring of TTP

A

slide 58 of lec 2

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43
Q

Do humans have PDC?; why or why not?

A

NO; bc if we did this, we would have a hangover after we worked out (acetylaldehyde is why we have hangovers)

**Vigorous exercise ⥇ Ethanol
** Acetaldehyde is toxic

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44
Q

Do humans have Alcohol Dehydrogenase?

A

YES!! (reversible)
➥ can turn ethanol into acetaldehyde
➤ Destroys ethanol made by intestinal bacteria
➤ Exogenous EtOH → acetaldehyde → hangover
➤ form of ADH partially determines susceptibility to aerodigestive cancers

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45
Q

What drug inhibits the reaction of Acetaldehyde⇢Acetate? Why would you want to do that?

A

disulfiram “Antabuse”. This is used to treat alcoholism, as it gives you a massive hangover

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46
Q

____is a competitive inhibitor of ADH

____ is a competitive inhibitor of Ethylene Glycol (antifreeze)

A

*Fomepizole

  • Ethanol
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47
Q

PET scans use___

A

2’-[¹⁸F] fluoro-2-deoxyglucose
→ Glucose analog that can be phosphorylated but not further metabolized
→ ¹⁸F decays by omitting a positron

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48
Q

In liver, Fructokinase converts:

A

Fructose + ATP → F1P +Pi

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49
Q

What enzyme is used in the reaction
1.Ethanol⇢Acetaldehyde
and
2.Acetaldehyde⇢Acetate?
where are they found?

A
  1. Alcohol Dehydrogenase
    (Cytosol)
  2. Acetaldehyde Dehydrogenase
    (Acetate)
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50
Q

Warburg effect

A

Cancer cells oftern convert glucose☞lactate instead of oxidative phosphorylation even when oxygen is present

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51
Q

lactate DH function

A

reduces pyruvate to lactate using NADH

reversible

cori cycle

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52
Q

What symptoms come from TTP (Vit B1) deficinecy?

A

*Pain
*Paralysis
*Wasting
*Heart Failure

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53
Q

✦What is the function of PFK-2 in the regulation of F6P and F2,6BP?

✧What is the function of F2,6BPase in the regulation of F6P and F2,6BP?

A

✦PFK-2 catalyzes the conversion of F6P to F2,6BP.

✧F2,6BPase catalyzes the conversion of F2,6BP back to F6P.

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54
Q

In an anabolic pathway, where do you get the energy you need to proceed the reaction

A

NADPH

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55
Q

what is the reaction that occurs between NAD+ and NADH ?

A

dehydrogenase reaction

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56
Q

pyruvate decarboxylase requires

A

thiamine pyrophosphate (TPP)

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57
Q

Hexokinase/Glucokinase (hormonal regulation)

A

✦ insulin stimulates/ activates HK & GK (indicates high blood glucose levels)

✧ Glucagon inhibits HK & GK (indicates low blood glucose levels)

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58
Q

Phosphofructokinase (Hormonal regulation)

A

✦ ** insulin** stimulates PFK II & inhibits F2,6BPase (glycolysis)

✧ Glucagon stimulates F2,6BPase and inhibits PFKII (GNG)

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59
Q

Pyruvate Kinase (Hormonal regulation)

A

✦ Insulin stimulates (dephosphorylase of PK)

✧ Glucagon inhibits (by phosphorylation of PK)

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60
Q

in ___, fructokinase converts:

A

liver; Fructose + ATP➔ F1P + Pi

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61
Q

Draw fructose metabolism

A

lec 2, slide 81

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62
Q

phosphofructokinase (PFK1) is also strongly activated by___? explain how

A

F2-6,BP

PFK-2 is responsible for the production of (F2,6BP), which is a potent allosteric activator of PFK-1. F2,6BP enhances the activity of PFK-1, thus stimulating glycolysis, and it inhibits the enzyme F1,6-BPase, which is involved in gluconeogenesis

(PFK2 –activates–> F2,6BP–activates–> PFK1 ➥ inhibits F1,6BPase
(F1,6BP is a product of it)

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63
Q

What enzyme is deficient in Johnny, causing him to dislike sweets?

A

Johnny has a deficiency in fructose-1-phosphate aldolase (F1P aldolase), also known as aldolase B.

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64
Q

What happens to fructose in Johnny’s body due to the lack of F1P aldolase?

A

Fructose is converted into fructose-1-phosphate (F1P), which accumulates due to the lack of F1P aldolase

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65
Q

How does the accumulation of F1P affect ATP and AMP levels? (why Johnny may not like sweets)

A

The accumulation of F1P leads to depletion of Pi, which reduces ATP production and increases AMP levels.

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66
Q

What effect does increased AMP and decreased ATP have on glycolysis? (johnny n sweets)

A

Increased AMP and decreased ATP stimulate glycolysis, leading to increased production of pyruvate and lactate, causing lactic acidosis.

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67
Q

How does the buildup of F1P affect blood glucose levels?

A

The depletion of Pi blocks glycogen breakdown, leading to low blood glucose levels (hypoglycemia).

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68
Q

What long-term effects can occur due to F1P accumulation in the body? (johnny n sweets)

A

Over time, the accumulation of F1P and associated metabolic disruptions can lead to liver and kidney damage, and in extreme cases, it can be fatal

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69
Q

What metabolic product causes Johnny to feel unwell after consuming sweets?

A

Johnny feels unwell because of the accumulation of lactate, which leads to lactic acidosis and a drop in blood pH.

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70
Q

Why is Pi depletion significant in Johnny’s metabolic disturbance?

A

Pi depletion limits ATP synthesis and blocks glycogen breakdown (glycogen → G1P), causing energy imbalances and low blood glucose.

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71
Q

How does fructose-1-phosphate (F1P) affect glucose metabolism?

A

Fructose-1-phosphate (F1P) facilitates glucose uptake by activating glucokinase, enhancing glucose’s entry into glycolysis.

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72
Q

What are the downstream products of fructose metabolism that are rapidly produced due to the bypass of PFK-1?
Answer:

A

Pyruvate and lactate are the downstream products rapidly produced due to the bypass of PFK-1.

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73
Q

What role does insulin play in fructose metabolism?

A

Insulin activates some glycolytic enzymes, enhancing glucose metabolism, but fructose largely bypasses these regulatory effects due to its detour around PFK-1.

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73
Q

How does fructose metabolism contribute to fat production?

A

Fructose metabolism increases pyruvate production, which is converted to acetyl-CoA. Excess acetyl-CoA is diverted to fatty acid synthesis, contributing to fat buildup.

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74
Q

Draw Galactose metabolism

A

Lec 2, slide 89

75
Q

Galactosemia

A

*Galactokinase deficiency
* buildup Gal→ galactinol→ cataracts

76
Q

GAL-1-P uridylyl transferase deficiency

A

❆ Gal-1-P→ toxic byproducts
❆ cataracts, liver damage, mental retardation
❆ can be fatal even on low gal diet

77
Q

UDP-4-epimerase deficiency

A

✭ Gal-1-P & UDG Gal → toxic byproducts
✭ cataracts, liver damage, mental retardation
✭ less severe with low gal diet

78
Q

draw mannose mechanism and explain what is happening

A

lec 2, slide 92
*Mannose, which differs from glucose in stereochemistry at carbon 2, is converted to mannose-6-P by hexokinase and then to F6P by an isomerase

79
Q

T/F; glycerol can also enter glycolysis pathway?

explain how or how not

A

*Glycerol is produced in substantial amounts during degradation
➥ Glycerol kinase (liver)
* Glycerol + ATP → Glycerol-3P + ADP
– Irreversible
➥ Glycerol-3P DH
* Glycerol-3P + NAD+ → DHAP + NADH

80
Q

Draw the Pentose Phosphate Pathway

A

Lec 2, slide 95

81
Q

T/F, the top section of PPP makes 2 NADH

A

FALSE; it makes 2 NADPH

G6P→ 5C sugar-P

82
Q

bottom section interconverts 3what type of sugars?

A

3C-7C sugars; NOT 2

83
Q

The top part of PPP is ____, while the bottom section is____.

A

irreversible (only operates when cell needs to make NADPH); reversible

84
Q

How does NADH and NADPH differ?

A

NADH:
* mainly in oxidized form (NAD+)
* removes 2 e- during “fuel” metabolism

NADPH:
* mainly in reduced form (NADPH instead of NADP+)
* adds 2e- during biosynthesis & detox of free radicals

85
Q

G6PDH is ____ and inhibited by high concentrations of____?

*what does G6P–> 6-phosphogluconolactone look like?

A

irreversible; NADP**H

*ring form of aldehyde⇨ ring form of carboxylic acid=lactone

86
Q

T/F you should put fructose on an IV drip for better hydration

A

FALSE; fructose is primarily metabolized on the liver, and rapid or excessive fructose infusion can overwhelm the liver’s metabolic capacity.

87
Q

T/F; hydrolysis of lactone occurs only enzymatically

A

FALSE; it occurs both enzymatically and non enzimatically

88
Q

T/F, 3 to 7 carbon sugars on PPP can be reversibly inter-converted without any pieces left over.

A

TRUE! 2 carbon metabolism is different

89
Q

how is xylulose similar to fructose in PPP?

A

C#2 of xylulose has =O and -OH of C#3 is “flipped to the other side” just like in fructose

90
Q

How does NADPH acts as an antioxidant?

A
  • Inactivates peroxides etc.
  • Reduces free radical damage
91
Q

G6P DH is a major source of ???
✦ what are the results of inactive G6P DH?

A

NADPH

✧Inactive G6P DH:
* ↑↑ peroxides
* Lipid and protein damage
* RBC lysis etc.
* Embryo death

92
Q

How does G6PD deficiency affect sensitivity to free radicals?

A

G6PD deficiency increases sensitivity to free radicals, especially from sources like fava beans and antimalarial drugs (such as primaquine), which lead to increased peroxide levels.

93
Q

What is the consequence of increased peroxide levels in people with G6PD deficiency?

A

Increased peroxide levels can lead to red blood cell lysis, resulting in anemia.

94
Q

Is anemia caused by G6PD deficiency permanent?

A

No, the anemia is transient; the body eventually produces new red blood cells with higher G6PD levels.

95
Q

Where is G6PD deficiency most common, and why?

A

G6PD deficiency is most common in regions where malaria is endemic, such as the Middle East and Africa. The deficiency offers partial protection against malaria, which provides a selective advantage in these areas.

96
Q

Xyl5P also activates___ in___?

A

PFK2 in liver

➥ after high carb meal
Pentose P pathway backs up
↑Xyl5P
↑F2,6BP
↑glycolysis
↑ Acetyl-CoA
↑FAT synthesis

97
Q

Why do cancer cells require large amounts of NADPH?

A

Cancer cells require large amounts of NADPH to fuel their anabolic processes, neutralize oxidative stress, synthesize essential biomolecules, and maintain rapid proliferation. NADPH supports both biosynthetic needs and antioxidant defense mechanisms, enabling cancer cells to thrive under conditions that would normally be harmful to regular cells

98
Q

Which tumor suppressor inhibits G6P DH in cancer cells?

A

p53

99
Q

What additional action does p53 have in relation to glycolysis?

A

p53 increases levels of TIGAR (an enzyme that acts as an F2,6BPase), reducing glycolysis.

100
Q

How does TIGAR affect glycolysis and the Warburg effect?

A

Answer: TIGAR reduces the level of F2,6BP, which decreases glycolysis, thus inhibiting the Warburg effect.

101
Q

Why are glycogen and gluconeogenesis important for maintaining blood glucose levels?

A

Glycogen stores and gluconeogenesis are essential because humans use approximately 160 grams of glucose per day, with the brain consuming 75%. Glycogen provides a reservoir of glucose, and gluconeogenesis in the liver and kidneys ensures glucose availability during fasting or low-carb diets.

102
Q

How much glucose can the human body store in glycogen and body fluids?

A

The body fluids contain about 20 grams of glucose, while glycogen stores can provide 180-200 grams.

103
Q

What is the role of glycogen in the liver during fasting or exercise?

A

The liver stores glycogen to maintain stable blood glucose levels (~5mM). During fasting or exercise, glycogen is broken down to provide glucose for the brain and other organs.

104
Q

How to get glucose if you are starving or on a low carb diet?

A

Fatty acids, but you get little if any glucose

Protein→ amino acids
→ pyruvate et. al
→ glucose

lactic acid → glucose

105
Q

What happens in muscle during strenuous exercise in terms of glycogen metabolism?

A

Muscles break down their glycogen stores (1-2% glycogen) to quickly mobilize glucose for energy during fight or flight responses or strenuous exercise

106
Q

How is the liver in terms of Glycogen metabolism?

A

Liver: up to 10% glycogen
❁ maintain ≈5 mM blood glucose
∼ brain normally uses only glucose (<2mM → pass out)
❁Liver has ≈ 16-hour supply of glucose
∼Supplement with gluconeogenesis
* Amino acids → glucose
* Fatty acids → little if any glucose

107
Q

where is brain glycogen mainly stored?

A

astrocytes

108
Q

How is glycogen in the brain different from glycogen in the liver and muscle?

A

Glycogen in the brain is rapidly mobilized in oxygen-limited conditions, such as during hypoxia, and it is often not detected because of its rapid use

109
Q

What role does glycogen in astrocytes play in the brain?
Answer:

A

Glycogen in astrocytes helps the brain cope with hypoxia and is also involved in processes like learning and memory.

110
Q

How does glycogen accumulate and mobilize in the brain compared to the liver?

A

Glycogen levels near neurons decrease while awake and increase during sleep. But during the day when you’re eating, glycogen levels rise in liver, whilr go down at night, bc you’re releasing glucose

111
Q

Why does brain glycogen play an important role despite being present in small amounts?

A

Even in small amounts, brain glycogen is important because it provides rapid energy under stress conditions (e.g., hypoxia) and supports cognitive functions like learning and memory.

112
Q

describe the glycogen structure

A

▶︎has ONE reducing end
▶︎MULTIPLE non reducing ends
branched
▶︎12 concentric shel

113
Q

What enzyme is responsible for breaking down glycogen, and what does it produce?

A

Glycogen phosphorylase is responsible for breaking down glycogen, and it produces glucose-1-phosphate (G1P).

114
Q

What cofactor does glycogen phosphorylase require for its activity?

A

Vitamin B6 (pyridoxal phosphate) for its activity.

115
Q

How does glycogen phosphorylase remove glucose units from glycogen?

A

Glycogen phosphorylase removes one glucose unit at a time from the non-reducing end of glycogen, provided it is at least 5 units away from a branch point.

116
Q

What is the advantage of using inorganic phosphate (Pi) in the cleavage reaction catalyzed by glycogen phosphorylase?

A

Using inorganic phosphate (Pi) for cleavage saves ATP because it directly produces G1P instead of requiring an additional phosphorylation step.

117
Q

Why is water excluded from the active site of glycogen phosphorylase?

A

Water is excluded from the active site to prevent hydrolysis of the glycogen chain, ensuring that glucose is released as G1P instead of free glucose.

118
Q

How is glycogen phosphorylase regulated?

A

Glycogen phosphorylase is regulated through allosteric regulation and covalent modification. Allosteric effectors like G6P and AMP shift its equilibrium between the T (inactive) and R (active) states. Hormones also regulate it via phosphorylation.

119
Q

What is the role of the debranching enzyme in glycogen metabolism?

A

The debranching enzyme transfers all but the last glucose unit from a branch to a nearby non-reducing end. It also cleaves the α-1,6 bond of the remaining glucose, releasing it as free glucose.

120
Q

The debranching cleaves at ___ bonds while the branching cleaves at___

A

debranching:

121
Q

What is the overall yield of glucose types when glycogen is broken down?

A

Approximately 90% of the glucose released from glycogen is in the form of G1P, while about 10% is released as free glucose from branch points

122
Q

Why can’t glycogen phosphorylase remove glucose units close to branch points?

A

Glycogen phosphorylase cannot remove glucose units that are closer than 5 units from a branch because its structure restricts access to glucose residues near the branch point.

123
Q

Will the debranching enzyme cleave to G-1-P?

A

no!, bc it’s not down at the bottom of the hole to be protected

124
Q

Phosphoglucomutase in terms of glycogen metabolism

A

✷ G1P⇒G6P
✷ REVERSIBLE

✷ Phosphoglucomutase catalyzes the reversible conversion between glucose-1-phosphate (G1P) and glucose-6-phosphate (G6P).

✷During glycogenolysis (glycogen breakdown), G1P (produced from glycogen by glycogen phosphorylase) is converted into G6P, which can then enter glycolysis for energy production or be dephosphorylated to free glucose in the liver.
During glycogenesis (glycogen synthesis), G6P is converted into G1P, which is then activated to UDP-glucose for incorporation into glycogen.

125
Q

How do glycogen phosphorylase and the debranching enzyme work together during glycogen breakdown?

A

❁Glycogen Phosphorylase initiates glycogen breakdown by cleaving α-1,4 glycosidic bonds at the non-reducing ends of glycogen, releasing glucose-1-phosphate (G1P). It continues this process until it reaches a point 4 glucose residues away from a branch point (α-1,6 linkage).
❁At this point, glycogen phosphorylase cannot proceed further, and the debranching enzyme takes over. The debranching enzyme has two activities:
☞Transferase Activity: It transfers a block of 3 glucose residues from the branch to a nearby non-reducing end, forming a new α-1,4 linkage.
☞Glucosidase Activity: It then cleaves the remaining single glucose unit attached by the α-1,6 bond, releasing it as free glucose.

126
Q

G6Pase

A

✴︎ liver ONLY
✴︎ G6P ➔ Gluc + Pi
✴︎ irreversible
✴︎ high Km
✴︎ allows excess glucose from glycogen breakdown or gluconeogenesis to enter the blood stream (for brain etc)

127
Q

What are the effects of G6Pase deficiency ?

A

In Von Gierke’s disease, individuals can store glycogen but cannot release glucose into the bloodstream. This leads to hypoglycemia (low blood glucose), requiring frequent feeding or continuous feeding via IV or gastric tube

128
Q

What are the effects of liver glycogen phosphorylase deficiency?

A

✷ Hers’ disease
☞ Difficult in mobilizing liver glycogen
∼Hypoglycemia

solution:
☞ frequent feeding
☞surgical transposition of portal vein

129
Q

What happens in muscle glycogen phosphorylase deficiency ?

A

In McArdle’s disease, individuals have difficulty mobilizing muscle glycogen, leading to painful cramps during strenuous exercise.

130
Q

What happens if you have a debranching enzyme deficiency?

A

✴︎Cori’s disease
✴︎ Can only mobilize glucose from ends of outer layer of glycogen ( can mobilize part of it but not all of it)
→ frequent feeding
→ high protein diet

131
Q

What are the key regulatory enzymes in glycogen metabolism?

A

✴︎glycogen phosphorylase, which breaks down glycogen, and ✴︎glycogen synthase, which synthesizes glycogen. These enzymes are regulated by allosteric factors and covalent modification.

132
Q

What enzyme catalyzes the rate-limiting step of gluconeogenesis, converting fructose-1,6-bisphosphate to fructose-6-phosphate?

A

The enzyme is fructose-1,6-bisphosphatase (F1,6BPase), which is allosterically regulated by AMP and fructose-2,6-bisphosphate (F2,6BP).

133
Q

What is the role of UDP-glucose pyrophosphorylase in glycogen synthesis?

A

UDP-glucose pyrophosphorylase converts glucose-1-phosphate (G1P) and UTP into UDP-glucose (UDP-G) and pyrophosphate (PPi)

134
Q

How is the reaction catalyzed by UDP-glucose pyrophosphorylase made irreversible?

A

The reaction is made irreversible by the hydrolysis of PPi to 2 Pi by the enzyme inorganic pyrophosphatase, which provides additional energy to drive the reaction forward.

135
Q

How many phosphate groups are involved in the formation of UDP-glucose?

A

Four phosphate groups are involved (three from UTP and one from G1P).

136
Q

Does glycogen synthesis directly require ATP in this step involving UDP-glucose?

A

No, ATP is not directly required in this step; instead, UTP is used to form UDP-glucose.

137
Q

Which enzymes are involved in glycogen degradation?

A

Glycogen phosphorylase removes glucose units from glycogen, and the debranching enzyme helps break down the branch points

138
Q

What is the role of phosphoglucomutase in glycogen metabolism?

A

Phosphoglucomutase converts glucose-1-phosphate (G1P) into glucose-6-phosphate (G6P), which can enter glycolysis or other metabolic pathways.

139
Q

Why is the hydrolysis of PPi to 2 Pi important in glycogen metabolism?

A

The hydrolysis of PPi to 2 Pi by inorganic pyrophosphatase ensures that the synthesis of UDP-glucose is irreversible, making the glycogen synthesis pathway energetically favorable.

140
Q

Why is the formation of UDP-glucose considered to have a high-energy bond, and how does it drive glycogen synthesis?

A

The formation of UDP-glucose involves a high-energy phosphoester bond between the UDP (uridine diphosphate) and glucose. This bond is considered high-energy because when it is cleaved, it releases enough energy to drive the addition of glucose to the growing glycogen chain. The energy released from breaking this bond makes the transfer of glucose by glycogen synthase to the glycogen molecule thermodynamically favorable, allowing glycogen synthesis to proceed.

141
Q

Glycogen synthase is____ under physiological conditions and adds to ____end

A

irreversible; nonreducing (C#4)

142
Q

Glycogen synthesis requires a primer, which is___

A

Glycogenin.
➥ Glycogenin is a self-glucosylating protein that serves as the core primer for glycogen synthesis. It has an attached tyrosine residue that catalyzes the attachment of the first glucose molecule from UDP-glucose to itself

143
Q

What are the effects of liver glycogen synthase deficiency?

A

✧little if any glycogen in liver

➥ ↑↑↑ blood sugar after eating
✧ low blood sugar at other times, usually early death

144
Q

Branching enzyme deficiency

A

Anderson’s disease
➥ normal amount of glycogen
➥ long unbranched chains
‣ low availability (less nonreducing ends)
‣ low solubility
‣autoimmune attack
‣ few survive past age 4

145
Q

Glycogen phosphorylase and synthase in terms of allosteric regulation:

A

Glycogen synthase
➥ ➕ G6P

Glycogen phosphorylase
➥➕ AMP
➥➖ ATP
➥➖ G6P
➥➖ Gluc

146
Q

what happens if there is excess sugar and energy vs low sugar and high energy demand in terms of *G6P, *ATP, *AMP?

A

excess sugar and energy:
↑ G6P, ↑ATP, ↓ AMP
→ make GLYCOGEN

low sugar & high energy demand:
↓ G6P, ↓ATP, ↑AMP
→ break glycogen down

147
Q
A
148
Q

How does epinephrine (adrenaline) affect glycogen metabolism?

A

Epinephrine increases cAMP levels, activating glycogen phosphorylase to mobilize glycogen and release glucose for energy during the “fight or flight” response.

149
Q

What role does glucagon play in glycogen metabolism?

A

Glucagon is released during low blood sugar levels, increasing cAMP in the liver, which activates glycogen phosphorylase to break down glycogen and release glucose into the bloodstream, especially to supply the brain

150
Q

How does insulin regulate glycogen metabolism?

A

Insulin is released during high blood sugar levels and works by decreasing cAMP levels, which promotes the activation of glycogen synthase to store glucose as glycogen and inhibit glycogen breakdown.

151
Q

What is the effect of increased cAMP in glycogen metabolism?

A

Increased cAMP leads to the activation of protein kinase A (PKA), which activates glycogen phosphorylase and stimulates glycogen breakdown.

152
Q

How does the hormonal regulation of glycogen metabolism differ between epinephrine/glucagon and insulin?

A

Epinephrine and glucagon increase cAMP,(in liver) leading to glycogen breakdown (mobilization), while the pancreas secretes insulin, which decreases cAMP, promoting glycogen synthesis storage
IN LIVER!!!

153
Q

Draw gluconeogenesis

A

lec 2, slide 37

154
Q

F1,6BPase opposes____
how?

A

PFK1

F1,6BPase:
➖ AMP
➕ ATP
➕ citrate
➖ F2,6P

PFK1
➕ AMP
➖ ATP
➖ citrate
➕ F2,6P

154
Q

What enzymes differ in glycolysis vs gluconeogensis?

A

Glucose → Glucose-6-phosphate Glycolysisis: Hexokinase/Glucokinase:
GLuconeogenesis: Glucose-6-phosphatase

Fructose-6-phosphate → Fructose-1,6-bisphosphate Glycolysis: (PFK-1) Gluconeogenesis:Fructose-1,6-bisphosphatase

Phosphoenolpyruvate → Pyruvate Glycolysis: Pyruvate kinase Gluconeogenesis:Pyruvate carboxylase & PEPCK

155
Q

Pyruvate Carboxylase ONLY happens in:

A

The mitochondria

156
Q

What is the role of pyruvate carboxylase in gluconeogenesis?

A

✴︎Pyruvate carboxylase converts pyruvate into oxaloacetate (OAA) in the mitochondria,
✴︎This enzyme is activated by acetyl-CoA.
✴︎ Irreversible
✴︎ Requires biotin

157
Q

Pyruvate requires ___, which is vitamin___. This vitamin serves as a ____.
➥ explain how

A

biotin; B7; mobile CO2 carrier

➥Pyruvate carboxylase uses ATP to load CO2 onto biotin and then delivers it to pyruvate.

158
Q

What enzyme converts oxaloacetate (OAA) to phosphoenolpyruvate (PEP) in gluconeogenesis?

A

phosphoenolpyruvate carboxykinase (PEPCK)

159
Q

T/F; PEPCK uses ATP as its main energy source

A

FALSE!; PEPCK uses GTP (guanosine triphosphate) rather than ATP to convert oxaloacetate to phosphoenolpyruvate.

160
Q

Where does the conversion of pyruvate to oxaloacetate (OAA) occur in gluconeogenesis?

and then Where does the majority of gluconeogenesis occur after OAA is formed?

A

The conversion of pyruvate to oxaloacetate (OAA) occurs in the mitochondria.

The majority of gluconeogenesis occurs in the cytoplasm, where OAA is eventually converted to glucose.

161
Q

Why is there a problem with OAA transport during gluconeogenesis?
➥ and how does the cell solve this problem?

A

The problem is that OAA cannot directly cross the mitochondrial membrane to reach the cytoplasm where gluconeogenesis continues
➥ The cell converts OAA to malate or aspartate within the mitochondria. These molecules can cross the mitochondrial membrane, and once in the cytoplasm, they are converted back to OAA.

162
Q

Why is NADH needed in the cytoplasm for gluconeogenesis?

A

NADH is needed in the cytoplasm for the reduction step of converting 1,3-bisphosphoglycerate to glyceraldehyde-3-phosphate during gluconeogenesis.

163
Q

Where is most NADH produced in the cell?

A

Most NADH is produced in the mitochondria during processes such as the citric acid cycle and beta-oxidation.

164
Q

How does the cell solve the problem of needing NADH in the cytoplasm for gluconeogenesis?

A

The cell uses the malate shuttle: OAA is converted to malate, which carries the reducing equivalents (NADH) across the mitochondrial membrane. In the cytoplasm, malate is converted back to OAA, regenerating NADH in the process.

165
Q

Can you explain how liver responds to low blood glucose? (cascade of events)

A

low blood glucose
➥ INC. glucagon secretion
➥ INC. cAMP
➥ INC. enzyme phosphorylation
➥ activation of FBPase-2 and inactivation of PFK2
➥ Decreased f2,6P
➥ inhibition of PFK and activation of FBPase
➥ INC gluconeogenesis

166
Q
A
167
Q

Draw the Pyruvate DH rxn
is it reversible or irreversible?

A

Pyruvate + CoA + NAD+ → Acetyl-CoA + CO2 + NADH

**Irreversible

168
Q

What does pyruvate DH require?

A
  • TTP (Vitamin B1)
  • FAD/ FADH ( Vit. B2)
  • NAD/ NADH ( vit. B3)
  • Acetyl-CoA (Vit. B5)
  • Lipoic acid
169
Q

what is the most important molecule that fuels the TCA cycle

A

acetyl CoA

170
Q

where does the TCA cycle occur

A

mitochondrial matrix

171
Q

In pyruvate DH rxn, hydroxyethyl-TTP transfers H3C-(C=O) to…?

A

lipoic acid

172
Q

Draw TCA cycle

A

lec 4; slide 4

173
Q

T/F humans make an excess amount of lipoic acid, so our body has to do a different mechanism to get rid of the excess.

A

FALSE!!; humans can’t make lipoic acid, ie it is a vitamin

174
Q

What are these compounds?
-OOC-CH2-CH2-(C=O)-COOOOC-CH2-CH2-COO-

-OOC-CH2-(C=O)-COO-

-OOC-CH2-HCOH-COO-

-OOC-CH=CH-COO

A

a-KG

succinate

oxaloacetate

malate

fumarate

175
Q

Which enzymes in the TCA cycle:

*release CO2
*require FAD or NAD or lipoic acid, *are inhibited by arsenic
*produce isocitrate or fumarate or αKG or OXAC
*use Acetyl-CoA as a substrate
*use GTP as a substrate

A

Release CO₂?
★Isocitrate dehydrogenase (converts isocitrate to α-ketoglutarate)
★α-Ketoglutarate dehydrogenase (converts α-ketoglutarate to succinyl-CoA)

Require FAD, NAD, or lipoic acid and are inhibited by arsenic?
★α-Ketoglutarate dehydrogenase complex requires NAD and lipoic acid and is inhibited by arsenic.
★Succinate dehydrogenase requires FAD but is not directly affected by arsenic.

Produce isocitrate, fumarate, α-ketoglutarate, or oxaloacetate (OAA)?
★Citrate synthase produces citrate, which converts to isocitrate.
★Aconitase rearranges citrate into isocitrate.
★Isocitrate dehydrogenase converts isocitrate into α-ketoglutarate.
★Succinate dehydrogenase produces fumarate.
★Malate dehydrogenase converts malate to oxaloacetate.

Use Acetyl-CoA as a substrate?

Citrate synthase is the enzyme that uses acetyl-CoA and oxaloacetate to form citrate.

Use GTP as a substrate?
★Succinyl-CoA synthetase uses GTP in the conversion of succinyl-CoA to succinate.

176
Q

List the reversible vs irreversible enzymes in TCA cycle

A

Irreversible
✧Citrate Synthase
✧Isocitrate Dehydrogenase ( 1st NADH)
✧α-Ketoglutarate Dehydrogenase ( 2nd NADH)

Irreversible
✦Aconitase
✦Succinyl-CoA Synthetase (Succinyl-CoA Thiokinase)
✦Succinate Dehydrogenase
✦Fumarase
✦Malate Dehydrogenase

177
Q

Citrate synthase is fueled by?

A

Thioester bonds

178
Q

𝛼-KG DH has the same enzymatic mechanism and cofactors as____
the cofactors being…

A

pyruvate DH

➥ TPP
➥ H-S-CoA
➥ Lipoic acid
➥ NAD+
➥ FAD

179
Q

Succinyl-CoA synthetase harvests high energy thioester bond to…

A

GTP

180
Q

Succinate DH uses ___→___

A

FAD → FADH2 bc FADH2 has less energy than NADH

181
Q

T/F; fumarase rxn is a hydration rxn, not a redox rxn

A

TRUE; converts fumarate → malate by adding water. (no NADH NADH or FADH2)

182
Q

TCA cycle regulation

A

➖ NADH
➖ ATP

➕ Ca 2+ (muscle contraction)

183
Q

low levels of TCA cycle intermediates would also cause:

A

high levels of acetyl-CoA

184
Q

What are some examples of anaplerotic rxns?

A

✩Pyruvate Carboxylase Reaction:
Pyruvate + CO₂ + ATP → Oxaloacetate (OAA) + ADP + Pi

✩Transamination of Glutamate to α-Ketoglutarate:
Reaction: Glutamate ↔ α-Ketoglutarate + NH3

✩ Aspartate Transaminase Reaction:
Aspartate + α-Ketoglutarate ↔ Oxaloacetate + Glutamate

✩Propionyl-CoA to Succinyl-CoA Conversion:
Propionyl-CoA → Succinyl-CoA

✩Pyruvate to Malate:
Pyruvate + CO₂ + NAD(P)H → Malate + NAD(P)+

✩PEP —PEP carboxylase–>oxaloacetate
✩ pyruvate —malic enzyme–> L-malate

185
Q

Where is the Glyoxylate cycle found?

A

Plants
Bacteria
FUNgi

NOT animals

BIOCHEM 411 w/ Park (3 decks)

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