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FHB Exam 3 > Metabolism: Glycolysis > Flashcards

Metabolism: Glycolysis Flashcards

1
Q

What are the reduced and oxidized forms of NAD/NADH? What is the function of each?

A 
reduced = NADH (reducing agent donates H+ to substrate)
oxidized = NAD+ (oxidizing agent pulls H+ off substrate)
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2
Q

What are the reduced and oxidized forms of NAD/NADH? What is the function of each?

A 
reduced = NADH (reducing agent donates H+ to substrate)
oxidized = NAD+ (oxidizing agent pulls H+ off substrate)
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3
Q

What is the fuel preference for liver?

A

FA
glucose
AA

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4
Q

What is the fuel preference for adipose?

A

FA

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5
Q

What is the fuel preference for the heart?

A

FA

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6
Q

What is the fuel preference for the skeletal muscle?

A

at rest = FA

during activity = glucose

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7
Q

What is the fuel preference for the brain?

A 
NEEDS glucose => quickly dies
if none (starvation) = ketone bodies
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8
Q

List the number of calories you get from each macromolecule.

A 
CHO = 4 kcal/g
protein = 4 kcal/g
fat = 9 kcal/g
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9
Q

Define hypoglycemia and its effects.

A
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10
Q

Define hyperglycemia and its effects.

A

> 110mg/100mL

  • insulin intolerance/beta cell dysfunction, glucose intolerance, T2M
  • oxidative stress
  • lipotoxicity
  • osmotic burden
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11
Q

Define glycogenolysis.

A
  • breakdown of glycogen to increase blood glucose levels

- induced by glucagon and epinephrine

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12
Q

Define glycogenesis.

A
  • anabolism of glucose to create glycogen to store glucose

- induced by insulin

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13
Q

Define glycolysis.

A
  • breakdown of glucose to generate pyruvate/lactate and energy, and substrates for TCA cycle
  • induced by insulin and high BG
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14
Q

Define gluconeogenesis.

A
  • only in the liver
  • reversing glycolysis to generate glucose from pyruvate
  • induced by glucagon and epinephrine
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15
Q

What are the 3 stages of glycolysis? What is the main end-product of each?

A
  1. priming = F16BP
  2. splitting = GAP/DHAP
  3. oxidoreduction-phosphorylation stage = pyruvate
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16
Q

List the 3 main glycolytic enzymes.

A
  1. hexo-/glucokinase
  2. PFK1
  3. pyruvate kinase
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17
Q

List the main steps in glycolysis.

A
  1. glucose => G6P (hexo/glucokinase)
  2. G6P => F6P (isomerase)
  3. F6P => F16BP (PFK1)
  4. F16BP => DHAP/GAP (aldolase A)
  5. DHAP => GAP (isomerase)
  6. GAP => 13BPG (GAP dehydrogenase)
  7. 13BPG => 3-phosphoglycerate (phosphoglycerate kinase)
  8. 3-PG => 2-PG (mutase)
  9. 2-PG => PEP (enolase)
  10. PEP => Pyruvate (pyruvate kinase)
  11. Pyruvate => lactate (LDH)
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18
Q

List the main steps in glycolysis.

A
  1. glucose => G6P (hexo/glucokinase)
  2. G6P => F6P (isomerase)
  3. F6P => F16BP (PFK1)
  4. F16BP => DHAP/GAP (aldolase A)
  5. DHAP => GAP (isomerase)
  6. GAP => 13BPG (GAP dehydrogenase)
  7. 13BPG => 3-phosphoglycerate (phosphoglycerate kinase)
  8. 3-PG => 2-PG (mutase)
  9. 2-PG => PEP (enolase)
  10. PEP => Pyruvate (pyruvate kinase)
  11. Pyruvate => lactate (LDH)
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19
Q

What is the fuel preference for liver?

A

FA
glucose
AA

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20
Q

What is the fuel preference for adipose?

A

FA

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21
Q

What is the fuel preference for the heart?

A

FA

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22
Q

What is the fuel preference for the skeletal muscle?

A

at rest = FA

during activity = glucose

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23
Q

What is the fuel preference for the brain?

A 
NEEDS glucose => quickly dies
if none (starvation) = ketone bodies
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24
Q

List the number of calories you get from each macromolecule.

A 
CHO = 4 kcal/g
protein = 4 kcal/g
fat = 9 kcal/g
25
Q

Describe the regulation of pyruvate kinase.

A

via phosphorylation

  • F16BP, high BG, insulin promote dephosphorylation to active form (phosphoprotein phosphatase)
  • ATP, alanine, low BG, glucagon, epi promote phosphorylation to inactive form (PKA)
26
Q

Define hyperglycemia and its effects.

A

> 110mg/100mL

  • insulin intolerance/beta cell dysfunction, glucose intolerance, T2M
  • oxidative stress
  • lipotoxicity
  • osmotic burden
27
Q

Define glycogenolysis.

A
  • breakdown of glycogen to increase blood glucose levels

- induced by glucagon and epinephrine

28
Q

Describe the effects of Pyruvate Carboxylase deficiency.

A
  • genetic
  • increased accumulation of alanine, lactate, pyruvate
  • developmental delay, seizures, acidosis
29
Q

Define glycolysis.

A
  • breakdown of glucose to generate pyruvate/lactate and energy, and substrates for TCA cycle
  • induced by insulin and high BG
30
Q

Define gluconeogenesis.

A
  • only in the liver
  • reversing glycolysis to generate glucose from pyruvate
  • induced by glucagon and epinephrine
31
Q

What are the 3 stages of glycolysis? What is the main end-product of each?

A
  1. priming = F16BP
  2. splitting = GAP/DHAP
  3. oxidoreduction-phosphorylation stage = pyruvate
32
Q

List the 3 main glycolytic enzymes.

A
  1. hexo-/glucokinase
  2. PFK1
  3. pyruvate kinase
33
Q

What are the 4 enzymes utilized for gluconeogenesis?

A
  1. pyruvate => oxaloacetate via pyruvate carboxylase
  2. oxaloacetate => PEP via PEP carboxykinase
  3. F16BP phosphatase
  4. G6P phosphatase
34
Q

List the main steps in glycolysis.

A
  1. glucose => G6P (hexo/glucokinase)
  2. G6P => F6P (isomerase)
  3. F6P => F16BP (PFK1)
  4. F16BP => DHAP/GAP (aldolase A)
  5. DHAP => GAP (isomerase)
  6. GAP => 13BPG (GAP dehydrogenase)
  7. 13BPG => 3-phosphoglycerate (phosphoglycerate kinase)
  8. 3-PG => 2-PG (mutase)
  9. 2-PG => PEP (enolase)
  10. PEP => Pyruvate (pyruvate kinase)
  11. Pyruvate => lactate (LDH)
35
Q

Describe the reaction carried out by hexokinase.

A
  • occurs in all cells
  • irreversible (require G6P phosphatase to reverse)
  • locks glucose in G6P (can’t leave cell)
  • low Km, high affinity (easily maximized at normal physiological levels)
  • constant amount
  • insulin independent
  • allosteric negative feedback inhibition by G6P
36
Q

Describe the reaction carried out by glucokinase.

A
  • only occurs in the liver and pancreas
  • insulin dependent
  • high Km, low affinity (phosphorylates in proportion to the amount in the blood)
  • in the nucleus (inactive); in the cytosol (active)
  • F6P promotes translocation to nucleus (no longer needed; have enough)
  • glucose promotes translocation to the cytosol (needed for glycolysis)
37
Q

Describe the function of PFK2.

A
  • converts F6P to F16BP
  • bifunctional (kinase and phosphatase, but never both at the same time)
  • irreversible
38
Q

What factors affect F16BP levels?

A
  • activators = insulin, high BG

- inhibitors = glucagon, epinephrine, low BG

39
Q

Describe the relationship between F16BP and PFK1.

A

F16BP activates PFK1 to promote glycolysis

40
Q

Describe the mechanism of glucagon/epinephrine inhibition of PFK2 in the liver.

A
  1. glucagon/epi => cAMP => PKA => phosphorylation of kinase domain of PFK2
  2. kinase activity is inhibited, phosphatase activity is activated
  3. F16BP is converted to F6P
  4. PFK1 is inhibited
  5. glycolysis is inhibited
41
Q

Describe the mechanism of glucagon/epinephrine effect on PFK2 in the heart and skeletal muscle.

A

NOTE: only the liver is affected by glucagon

  1. epi => cAMP => PKA => phosphorylation of phosphatase domain of PFK2
  2. phosphatase activity is inhibited, kinase activity is activated
  3. F6P is converted to F16BP
  4. PFK1 is activated
  5. glycolysis is activated
42
Q

Describe the regulation of pyruvate kinase.

A

via phosphorylation

  • F16BP, high BG, insulin promote dephosphorylation to active form (phosphoprotein phosphatase)
  • ATP, alanine, low BG, glucagon, epi promote phosphorylation to inactive form (PKA)
43
Q

List the 4 fates of pyruvate.

A
  1. pyruvate => acetyl-CoA => TCA (via PDH)
  2. pyruvate => lactate (via LDH)
  3. pyruvate => oxaloacetate (via pyruvate carboxylase)
  4. pyruvate => alanine (via transaminase)
44
Q

Describe the effects of PDH deficiency.

A
  • genetic
  • increased pyruvate and lactate accumulation
  • microcephaly, mental retardation, poor muscle coordination
45
Q

Describe the effects of Pyruvate Carboxylase deficiency.

A
  • genetic
  • increased accumulation of alanine, lactate, pyruvate
  • developmental delay, seizures, acidosis
46
Q

Why is the NAD+/NADH ratio so important? How is it maintained?

A
  • NAD+ is present in little amount in the cytoplasm. It needs to be regenerated in order for glycolysis to continue.
  • anaerobic: reduction of pyruvate to lactate or ethanol regenerates NAD+ (LDH)
  • aerobic: mitochondrial metabolite shuttle system (malate asparatate or glycerol phosphate), ETC
47
Q

What processes require oxygen (aerobic)?

A
  • pyruvate dehydrogenase activity (reoxidation of NADH)

- metabolic shuttle in mitochondria

48
Q

Describe the lactate dehydrogenase reaction.

A

pyruvate + NADH lactate + NAD+

  • if you have low levels of NADH, you will not be able to generate lactate
  • this is anaerobic
  • in muscles, prefer production of lactate
  • in heart, prefer production of pyruvate
49
Q

Describe the components of PDH.

A

E1, E2, E3

converts Pyruvate to acetyl-CoA

50
Q

Which vitamins are required for proper PDH activity?

A 
E1 = thiamin (B1 - in form of thiamine pyrophosphate)
E2 = lipoate CoA (B5 - pantothenate)
E3 = FAD/NAD (B2 - riboflavin, B3 - niacin)
51
Q

How is PDH regulated?

A

allosteric negative feedback inhibition

  • acetyl-CoA
  • NADH
52
Q

Describe the effects of a LDH deficiency.

A
  • genetic recessive
  • poor muscle control because can’t undergo glycolysis to make ATP
  • can’t regenerate enough NAD+
53
Q

What is the net ATP production of glycolysis?

A

2 ATP
2 NADH
2 H+
2 H2O

54
Q

How does galactose contribute to glycolysis?

A

galactose => galactose-1P (via galactokinase)

galactose-1P => glucose-1P (via gal-1P uridyltransferase)

55
Q

Which enzyme deficiencies cause galactosemia?

A
  • galactokinase

- gal-1P uridyltransferase (most common)

56
Q

What is the effect of galactosemia and the treatment?

A

genetic deficiency of enzymes

  • cataracts due to galactose accumulation => galactitol
  • galactosuria
  • if classic: hepatic dysfunction, brain dysfunction

tx: remove galactose from diet (remove lactose, milk)

57
Q

What is the function of aldolase B?

A

inserts fructose into the glycolysis cycle

58
Q

Describe hereditary fructose intolerance.

A
  • autosomal recessive deficiency of aldolase B
  • accumulation of fructose
  • hypoglycemia, vomiting, jaundice, hepatic failure
    tx: avoid fructose

FHB Exam 3 (23 decks)

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