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MCM Quiz 1 > Glycolysis > Flashcards

Glycolysis Flashcards

1
Q

What is the purpose of glycolysis?

A

1 molecule of glucose to 2 molecules of pyruvate and generates 2 molecules of ATP.

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2
Q

Where does glycolysis occur?

A

Occurs in cells that lack mitochondria (erythrocytes)

Important in overworked muscles that lack O2

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3
Q

Which parts of the body use glycolysis?

A
  • Glucose the only fuel that red blood cells can use

- Glucose the only fuel that brain uses under non-starvation conditions

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4
Q

First part of glycolysis?

A

transport of glucose into the cell using a transporter

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5
Q

What type of GLUTS are there and what do they do?

A
  • GLUT1: rbcs, high affinity
  • GLUT2: liver, low affinity
  • GLUT3: neurons, high affinity
  • GLUT4 : skeletal tissue, heart, adipose tissue: insulin dependent
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6
Q

What is the significance of GLUT4?

A
  • Insulin signaling, fusion of vesicles, insertion of transporter in membrane
  • increases GLUT4 uptake
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7
Q

What are the three phases of Glycolysis?

A
  1. Investment
  2. Splitting
  3. Recoup/Payoff
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8
Q

Explain the three steps of Phase 1, what their enzymes are and what + and - them?

A
  1. Glucose to G6P (hexokinase or glucokinase)
    * ATP
    * Regulatory
  2. G6P to F6P (phopsoglucose isomerase)
  3. F6P to F1,6BP (PFK1)
    * ATP
    * Rate limiting
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9
Q

What are the steps of Phase 2, their enzymes and what + and - them?

A
  1. F1,6BP forms DHAP and G3P (Aldolase A)

5. Isomerization of DHAP to G3P (Triose phosphate isomerase)

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10
Q

What are the steps of phase 3, what enzymes and what + and - them?

A
  1. Phosphorylation of G3P (GAPDH)
    * NAD to NADH
  2. 1,3BPG to 3PG (Phosphoglycerate kinase)
    * ADP becomes ATP
  3. Pyruvate formed (Pyruvate kinase)
    - irreversible
    * ADP becomes ATP
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11
Q

Checkpoints of Glycolysis , what are they? what are they influenced by?

A
  1. hexokinase/glucokinase
  2. PFK1
  3. pyruvate kinase
    - influenced by ATP, AMP, Glucose, Insulin, Glucagon
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12
Q

Where is hexokinase present? whats special about it?

A

-in all cells

–Highaffinity, functional even at low [glucose]–Inhibited by G6P (product)

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13
Q

Where is glucokinase? whats special about it?

A

-Liver and pancreatic b cells

–Lowaffinity for glucose, Weakly inhibited by G6P

–Most active when high [glucose], i.e. after meal

–F6P promotes translocation to nucleus

–Sequestered by GK-Regulatory Protein

–High glucose promotes dissociation from GK-RP

–Followed by translocation to cytoplasm

–Insulin induces synthesis of GK and glucagon inhibits synthesis.

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14
Q

What is the rate limiting step in glycolysis and what activates it and stops it?

A
  • Activated AMP, F2,6BP

- inhibited by ATP, citrate

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15
Q

What is F2,6BP and what does it do?

A
  • PFK-2/FBPase-2 is a bifunctional enzyme that works as a kinase in its dephospho form and phosphatase in its phospho form.
  • dephospho form favored by insulin
  • phospho form favored by glucagon
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16
Q

How does F2,6BP work?

A
  • .High insulin/low glucagon: activate protein phosphatases, dephosphorylate PFK-2/FBPase-2 producing F2,6BP which activates PFK-1
  • High glucagon/low insulin: induces high [cAMP], activate protein kinase A, phosphorylates PFK-2/FBPase-2 , reduces PFK-1 activity.
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17
Q

What is Tarui Disease

A

-Deficiency in PFK-1

-–Exercise-induced muscle cramps and weakness
–Hemolytic anemia
–High bilirubin and jaundice

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18
Q

How is pyruvate kinase regulated?

A
  • Activated by F1,6BP and insulin
  • Inhibited by ATP, Alanine, and glucagon
  • High insulin: stimulates protein phosphatase, dephosphorylation of PK, activate
  • High glucagon: cAMP activates PKA, phosphorylation, PK inhibited.
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19
Q

What other pathways is G6P used for ?

A
  • Pentose phosphate pathway
  • galactose metabolism
  • glycogen synthesis
  • uronic acid pathway
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20
Q

What contributes to pyruvate? Where is pyruvate used?

A
  • Glucose, tryptophan, threonine , alanine make pyruvate

- pyruvate makes Acetyl Coa, Alanine, Oxaloacetate, Lactate, Alanine

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21
Q

What is the only fuel that can cross the BBB?

A

Glucose

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22
Q

During extreme starvation, what does the brain use for fuel?

A

ketone bodies

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23
Q

What is hemolytic anemia ?

A

Premature death of RBCs, often due to issues with glycolysis

Clinical markers: elevated lactate dehydrogenase, unconjugated bilirubin

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24
Q

Fanconi-Bickel syndrome what is it?

A

mutation in GLUT 2 transporter, autosomal recessive

Unable to take up glucose, fructose and galactose

Treatment – vitamin D and phosphate, and uncooked corn starch

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25
Q

What is gluconeogenesis? where does it occur?

A
  • makes glucose out of pyruvate
  • occurs when glucose and glycogen stores are done
  • liver, kidney, and small intestine
  • Major precursors are lactate, amino acids, and glycerol
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26
Q

Which enzymes are used in gluconeogenesis to bypass glycolysis

A
  • Pyruvate carboxylase
  • Phosphoenolpyruvate carboxykinase
  • Fructose 1,6-bisphosphatase
  • Glucose 6-phosphatase
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27
Q

What are the + and - regulators of gluconeogenesis?

A

+ are Glucagon, citrate, cortisol, thyroxine, acetyl coa

-are ADP, AMP, Fru 2,6 BP

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28
Q

How is Pyruvate carboxylase regulated?

A
  • Mitochondrial enzyme, mot others are in cytoplasm
  • First step of gluconeogenesis, pyruvate forms oxaloacetate
  • needs Biotin cofactor, uses CO2 and ATP
  • Activated by Acetyl Coa and cortisol
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29
Q

How does the malate shuttle work?

A
  • OAA reduced to malate by mitochondrial malate dehydrogenase
  • malate sent to cytoplasm via malate shuttle
  • reoxidized to OAA by malate dehydrogenase
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30
Q

What does PEPCK do? how is regulated?

A

makes oxaloacetate to PEP

activated by cortisol, glucagon, thyroxine

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31
Q

What is Fructose 1,6-Bisphophatase ? what does it do?

A
  • rate limiting step of gluconeogenesis
  • F1,6BP to F6P

–Activated: cortisol and citrate
–Inhibited: AMP and F26BP

32
Q

What is Glucose 6-Phosphatase? what does it do?

A

-G6P becomes glucose

–Only in liver, kidneys, SI and pancreas
–Activated by cortisol

33
Q

What is so special about G-6phosphatase?

A
  • has 3 subunits: a catalytic unit, a glucose 6-phosphate and Pi antiporter, and a glucose transporter (GLUT7).
34
Q

What is the cori cycle? why is it so special?

A

-Links the lactate produced from anaerobic glycolysis in RBC and exercising muscle to gluconeogenesis in liver

–Prevents lactate accumulation
–Regenerates glucose

35
Q

What are the precursors of gluconeogenesis?

A

Carbs, lipids, proteins

36
Q

What is F1,6BP deficiency? what does it do?

A

-Hypoglycemia, lactic acidosis, ketosis, apnea, hyperventilation

37
Q

What is Von Gierke disease? what does it do?

A
  • Deficiency in glucose 6-phosphatase
  • Inefficient release of free glucose into the bloodstream by the liver in gluconeogenesis and glycogenolysis
  • Patients exhibit marked fasting hypoglycemia, lactic acidosis, hepatomegaly due to buildup of glycogen, hyperlipidemia and potentially retarded growth
38
Q

What is Glut 5 used to uptake?

A

Fructose

39
Q

What is SGLT 1 used to uptake?

A

glucose/galactose

40
Q

What can a lack of sorbitol dehydrogenase cost?

A

sorbitol won’t become fructose, cataracts

41
Q

What are the steps in galactose metabolism?

A

Galactose to Galactose1P via Galactokinase

Galactose1P to Glucose1P via GALT

42
Q

What is lactose intolerance?

A
  • Drinking milk causes disturbances in GI function

- Caused by deficiency in enzyme lactase

43
Q

Why can fructose lead to pathological conditions?

A
  • Actions of fructokinase and triose kinase bypass the most important regulatory step in glycolysis, the phosphofructokinase-catalyzed reaction
  • Fructose-derived G3P and DHAP are processed by glycolysis to pyruvate and acetyl CoA in an unregulated fashion.
  • Excess acetyl CoA converted to fatty acids, which can be transported to adipose tissue to form triacylglycerols, resulting in obesity
  • Fatty liver
44
Q

Deficiency in glucose 1P uridyltransferase (GALT) what is it?

A

Leads to accumulation of galactitol

45
Q

Deficiency in Galactokinase what is it ?

A

Leads to accumulation of galactose and galactitol in blood and urine

46
Q

What does the Pentose Phosphate pathway do?Where does it occur?

A

–Produces no energy but metabolizes glucose
–Produces the sugar for DNA and RNA formation
–Produces NADPH
-Occurs in the cytosol

47
Q

What are the two main things in PPP?What is the rate limiting step? What does it produce?

A
  • oxidation of G6P to Ribulose 5 phosphate
  • Reduction of NADP to NADPH

-rate limiting step is G6P to 6phosphogluconolactone (G6PD), makes 2 NADPH and 1 CO2

48
Q

What does G6PD deficiency do?

A

Presentation of hemolytic anemia when NADPH need is elevated

49
Q

in PPP, what is the purpose of gluthianone?

A

regenerates glutathione

detoxifies H2O2 with glutathione reductase

50
Q

What is the non oxidative phase of the ppp? what steps are there?

A
  • reversible reactions
  • End products shunt to glycolytic, gluconeogenic or nucleotide synthesis pathways
  • Carbon transfer via transketolase or transaldolase
51
Q

How is PPP modified based on cellular demand?

A
  • High demand of Ribose 5P: rapidly dividing cells oxidative phase favored to produce Ribulose 5P
  • High demand for NADPH: non-oxidative products channeled into gluconeogensis for re-entry into PPP
52
Q

What is the structure of glycogen?

A
  • Glucose molecules within chain linked together via α-1,4 glycosidic bonds
  • Branch points formed via α-1,6 glycosidic
  • Non-reducing ends each contain a terminal glucose with a free hydroxyl group at Carbon 4
  • Reducing end consists of glucose monomer connected to a protein called glycogenin
53
Q

On which end is glycogen degraded?

A

degraded and extendedfrom non-reducing end

54
Q

Where is glycogen stored?

A
  • in the liver, muscle as granules
55
Q

What is the difference between liver and muscle glycogen?

A
  • Liver glycogen - regulates blood glucose levels

- Muscle glycogen - provides reservoir of fuel (glucose) for physical activity

56
Q

What are the first step of glycogenesis? Include enzymes and what is produced

A
  1. Glucose to G6P (Hexokinase/Glucokinase)
    - ATP used

2.Glucose6P to Glucose1P (PGM)

  1. G1P to UDP Glucose (UDPglucosepyrophosphorylase)
    - 2 UTP used
57
Q

What are the second step of glycogenesis? Include enzymes and what is produced

A

Glycogen primer is elongated,

Glycogen synthase Catalyzes transfer of glucose from UDP-glucose to non-reducing end of glycogen chain

a1,4 bonds

58
Q

What is the rate limiting step of glycogenosis?

A

glycogen synthase

UDP Glucose to Glycogen

59
Q

What is the third step of glycogen synthase?

A
  • branching of glycogen chains

- a α -1, 4 link and reattached elsewhere via α -1, 6 link by glucosyl (4:6) transferase

60
Q

What are the two main steps of glycogenolysis? main enzymes and substrates

A
  1. Chain shortening :
    - Glycogen phosphorylase, cleaves g1p subunits from reducing end of glycogen
    - uses vitamin B6 as cofactor
    - gets with 4 residues of a1,6 branching point
  2. Branch transfer and release of glucose
    - debranching enzyme uses its transferase (4:4) activity to transfer a block of 3 of the remaining 4 glucose to the non-reducing end
61
Q

Liver vs. muscle glu 1 p

A
  • in liver, Glu-1-P converted to Glu-6-P by an epimerase and then to Glu by glucose-6-phosphatase. Free glucose released into blood stream
  • in muscle, s keletal and cardiac muscle lack glucose-6-phosphatase and can’t hydrolyze Glu-6-P. Use it to generate energy via glycolysis and TCA cycle
62
Q

Why is the regulation of glycogen metabolism importnat?

A
  • to maintain blood sugar

- to provide energy to muscle

63
Q

what is the rate limiting step of glycogen synthesis? degradation?

A

glycogen synthase, glycogen phosphroylase

64
Q

How does phosphorylation affect glycogen synthase and glycogen phosphorylase?

A

glycogen synthase:

–dephospho form active

–phospho form inactive

glycogen phosphorylase:

–dephospho form inactive

–phospho form active

65
Q

When is glycogenesis favored?

A

–blood glucose high
–insulin high
–cellular ATP high

66
Q

When is glycogenolysis favored?

A

–blood glucose low
–glucagon high

  • cellular calcium is high
  • AMP is high
67
Q

How is glycogen synthase/phosphorylase regulated by insulin?

A
  • Insulin binds to RTK
  • PKB activated
  • GLUT 4 translocated
  • PKB phosphorylates PP1( activated) and GSK3( inactivated)

Active PP1 dephosphorylates glycogen synthase (activate) and dephosphorylates glycogen phosphorylase (inactivate)

68
Q

How is glycogen synthase/phosphorylase regulated by glucagon?

A

Glucagon binds to GPCR on hepatocytes

  • turns on G protein
  • Activates AC which forms cAMP
  • Activates PKA
  • PKA phosphorylates glycogen synthase (inactivates)
  • PKA phosphorylates PK (activate)
  • PKA phosphorylates an inhibitor which inactivates PP1
  • Active PK phosphorylates glycogen phosphorylase (activates)
69
Q

Regulation by Epinephrine of glycogen?

A

–Fight or flight response
–Epinephrine released by adrenal glands
–Promotes degradation of glycogen
–Pathway similar to glucagon

70
Q

What is GSD 0?

A
  • Deficiency in glycogen synthase
  • Patients cannot synthesize and store glycogen
  • Have muscle cramps due to lack of glycogen in muscle
71
Q

GSD1a/Von Gierke disease?

A
  • Deficiency in glucose 6-phosphatase

- Inefficient release of free glucose into the bloodstream by the liver following gluconeogenesis and glycogenolysis

72
Q

GSD II/Pompe Disease?

A
  • Deficiency in Acid Maltase aka acid α -glucosidase
  • Impairs lysosomal glycogenolysis resulting in accumulation of glycogen in lysosomes
  • Disrupts normal functioning of muscle and liver cells
73
Q

GSD III/Cori Disease?

A
  • Deficiency in α-1,6,-glucosidase (debranching enzyme)

- Patients possess glycogen molecules with large number of short branches

74
Q

GSD IV/Andersen Disease

A
  • Deficiency in glucosyl (4:6) transferase (branching enzyme)
  • Patients have long chain glycogen with fewer branches
75
Q

GSD V/McArdle Disease?

A
  • Deficiency in muscle glycogen phosphorylase
  • Rate limiting step of glycogen breakdown
  • Patients unable to supply muscles with enough glucose
76
Q

GSD VI/Hers Disease?

A
  • Deficiency in liver glycogen phosphorylase

- prevents glycogen breakdown in liver, hence it accumulates in liver causing hepatomegaly

MCM Quiz 1 (9 decks)

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