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POM Exam 1 > L13: PPP, Glycogen Metabolism, and Alcohol Metabolism > Flashcards

L13: PPP, Glycogen Metabolism, and Alcohol Metabolism Flashcards

1
Q

main functions of pentose phosphate pathway

A
  • bypass first step in glycolysis
  • generate NADPH
  • generate ribulose-5-phosphate
  • provide precursors for nucleotide biosynthesis
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2
Q

NADPH role

A
  • reductive reactions required for biosynthesis
  • protection against oxidative stress
  • fatty acid synthesis
  • glutathione reduction
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3
Q

ribulose-5-phosphate role

A
  • nucleotide biosynthesis
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4
Q

oxidative phase

A
  • oxidation of glucose-6-phosphate to ribulose-5-phosphate
  • via glucose-6-phosphate dehydrogenase
  • produces 2 NADPH
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5
Q

non-oxidative phase

A
  • ribulose-5-phosphate to fructose-6-phosphate

- produces glycolytic pathway intermediates

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6
Q

Phase I regulation of PPP

A
  • high NADPH inhibits glucose-6-phosphate dehydrogenease
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7
Q

Phase II regulation of PPP

A
  • controlled by substrate availability
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8
Q

cancer cells and PPP

A
  • need nucleotides for DNA and RNA synthesis
    • so need ribose-5-phosphate
  • need NADPH for fatty acid synthesis
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9
Q

Why do we use glycogen for storage?

A
  • glucose cannot be stored by itself because it would disrupt the osmotic balance of the cell
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10
Q

alpha 1,4 linkage in glycogen

A
  • joins the glucose molecules in a linear molcule
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11
Q

alpha 1,6 linkage in glycogen

A
  • results in branches
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12
Q

why do we have branches in glycogen?

A
  • makes it much easier for enzymes involved in degradation to find something to degrade
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13
Q

function of glycogen in the muscle

A
  • serves as a fuel source
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14
Q

function of glycogen in the liver

A
  • serves as a good source of blood glucose for other tissues
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15
Q

energy requirements in glycogen synthesis versus breakdown

A
  • synthesis requires energy

- breakdown does not

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16
Q

glycogenolysis step 1

A
  • via phosphorylated glycogen phosphorylase
  • cleaves alpha 1,4 bonds, adds a phosphate
  • releases glucose-1-phosphate residues until only 4 residues remain
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17
Q

glycogenolysis step 2

A
  • transferase removes outer 3 glucose residues from a branch and transfers them to another chain
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18
Q

glycogenolysis step 3

A
  • alpha-1,6-glucosidase (branching enzyme) cleaves alpha-1,6 bond on the single residue
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19
Q

glycogenolysis step 4

A
  • glucose-1-phosphate converted to glucose-6-phosphate by phosphoglucomutase
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20
Q

liver versus muscle in glucose-6-phosphatase

A
  • liver breaks down glucose-6-phosphate to glucose via glucose-6-phosphatase in ER membrane
  • muscle uses glucose-6-phosphate to generate ATP
    • does not have phosphatase
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21
Q

important component of glycogen degradation

A
  • glycogen phosphorylase
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22
Q

hormones that control glycogen degradation

A
  • glucagon in the liver
  • epinephrine in the muscle
  • signal through GCPR pathway
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23
Q

when glucose levels are low

A
  • glucagon and epi released
  • GCPR pathway
  • cAMP made from ATP
  • activate PKA
  • activate phosphorylase kinase
  • inactivates glycogen synthase
  • phosphorylation of glycogen phosphorylase (a form) initiates glycogen degradation
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24
Q

step 1 of glycogen synthesis

A
  • glucose-6-phosphate -> glucose-1-phosphate

- via phosphoglucomutase

25
Q

step 2 of glycogen synthesis

A
  • glucose-1-phosphate -> UDP-glucose

- via UDP-glucose pyrophosphorylase

26
Q

step 3 of glycogen synthesis

A
  • glycogenin primes the initial synthesis of a short glucose chain using UDP-glucose as a substrate
27
Q

step 4 of glycogen synthesis

A
  • glycogen chain extended with more glucose

- via glycogen synthase and UDP-glucose

28
Q

step 5 of glycogen synthesis

A
  • glycogen branches creating by transferase (branching enzyme)
  • breaks 1,4 links and forms 1,6 links
    • occurs about every 12 residues
29
Q

important hormone in glycogen synthesis

A
  • glycogen synthase
30
Q

insulin signaling and glycogen storage

A
  • insulin released from pancreas
  • activates glycogen synthase kinase (a form)
  • activates phosphatase 1
  • removes phosphate from glycogen synthase, which activates it
31
Q

Type I glycogen storage disease

A
  • Von Gierke
32
Q

Von Gierke cause

A
  • defect in glucose-6-phosphatase
  • glucose can’t be transported from liver
  • glycogen accumulates in liver
  • excess glucose-6-phosphate results in high rates of glycolysis with high levels of lactate and pyruvate in the blood
33
Q

Von Gierke symptoms

A
  • massive liver enlargement
  • hypoglycemia
  • weakness
34
Q

Type II

A

Pompe Disease

35
Q

Pompe disease cause

A
  • defect in lysosomal alpha glucosidase that breaks down glycogen in lysosomes
  • leads to increased membrane bound glycogen
36
Q

Pompe disease symptoms

A
  • muscle and nerve damage
37
Q

Type III

A
  • Cori disease
38
Q

Cori disease cause

A
  • defect in debranching enzyme
  • increase of glycogen with short outer branches
  • can’t break down well
  • only a limited amount of glucose can be released
39
Q

Cori disease symptoms

A
  • like Von Gerke but milder
40
Q

Type IV

A
  • Andersen disease
41
Q

Andersen disease cause

A
  • defect in branching enzyme

- keep making longer branches

42
Q

Andersen disease symptoms

A
  • usually fatal

- liver can’t handle longer branches of glycogen

43
Q

Type V

A
  • McArdle disease
44
Q

McArdle disease cause

A
  • defect in muscle glycogen phosphorylase

- no glycogen metabolized

45
Q

McArdle disease symptoms

A
  • exercise induced muscle pain
  • cramps
  • weakness
46
Q

type VI

A
  • Hers disease
47
Q

Hers disease cause

A
  • defect in liver glycogen phosphorylase
48
Q

Hers disease symptoms

A
  • mild hypoglycemia

- hepatomegaly

49
Q

two pathways of alcohol metabolism

A
  • alcohol dehydrogenase - modest levels of ethanol

- MEOS - high levels of ethanol

50
Q

alcohol dehydrogenase system

A
  • alcohol dehydrogenase in liver oxidizes ethanol to acetaldehyde and generates NADH
  • acetaldehyde is converted to acetate by acetaldehyde dehydrogenase and generates NADH
  • acetate released into bloodstream for use by tissues
51
Q

acetaldehyde and drinking

A
  • acetaldehyde is the negative effects of drinking

- nausea, etc

52
Q

alcohol dehydrogenase

A
  • low Km for ethanol

- active at low ethanol concentrations

53
Q

ALDH2 human variants

A
  • have acetaldehyde dehydrogenase with low Km and low activity (Vmax)
  • low levels of ethanol result in nausea
54
Q

disulfiram

A
  • inhibits acetaldehyde dehydrogenase

- used to treat alcoholism

55
Q

MEOS system

A
  • metabolizes alcohol to acetaldehyde requiring NADPH

- highest activity is CYP2E1

56
Q

CYP2E1

A
  • high affinity
  • functions at high levels of alcohol consumption
  • results in increased production of free radicals and tissue damage
57
Q

result of NADH buildup in liver

A
  • fatty acid oxidation is inhibited
    • fat accumulation in liver
  • acetyl CoA shifted away from TCA cycle toward ketone body production
  • lactate dehydrogenase reaction shifted toward lactate production
58
Q

lactate dehydrogenase reaction shifted toward lactate production

A
  • lactic acidosis

- lactic acid competes with uric acid in kidney for excretion

59
Q

lactic acid competes with uric acid in kidney for excretion

A
  • decrease in uric acid excretion
  • uric acid crystals
  • gout!

POM Exam 1 (16 decks)

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