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MCM Exam 1 > Carbohydrate Metabolism > Flashcards

Carbohydrate Metabolism Flashcards

1
Q

GLUT 1

A

Ubiquitous, but high in RBCs and brain.

High affinity for Glc. (Unreg.)

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2
Q

GLUT 2

A

Main transporter in liver.

Low affinity for Glc. (Unreg.)

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3
Q

GLUT 3

A

Main transporter in neurons.

High affinity for Glc. (Unreg.)

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4
Q

GLUT 4

A

Present in skeletal muscle, heart and adipose tissue.

Insulin dependent.

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5
Q

More on GLUT 4:

A

Sequestered in vesicles.
Insulin signaling causes fusion of vesicle w/ PM.
Enables uptake of Glc.

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6
Q

3 Phases of Glycolysis

A
  1. Investment
  2. Splitting
  3. Payoff
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7
Q

Net Yield of Glycolysis

A

2 ATP, 2 NADH, 2 pyruvate

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8
Q

Investment Phase (3)

A
  1. Phosphorylation of Glc to G6P (use ATP)
  2. Isomerization of G6P to F6P
  3. Phosphorylation of F6P to F 1,6-BP (RLS and uses ATP)
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9
Q

Splitting Phase (2)

A
  1. Cleavage of F 1,6-BP (now two 3C molecules)

5. Isomerization

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10
Q

Payoff Phase (3)

A
  1. Phosphorylation of G3P (Reduces NAD+ to NADH x 2)
  2. Conversion of 1,3-BPG to 3-PG (1 ATP)
  3. Formation of pyruvate (1 ATP)
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11
Q

Enzymes Catalyzing ATP using/producing Reactions and Produce NADH

A
  1. Hexokinase/glucokinase - Glc to G6P (1 ATP)
  2. PFK-1 - F6P to F 1,6-BP (1 ATP)
  3. Glyceraldehyde 3-P DH - G 3-P to 1,3-BPG (2 NADH)
  4. Phosphoglycerate kinase - 1,3-BPG to 3-PG (1 ATP)
  5. Pyruvate kinase - PEP to pyruvate (1 ATP)
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12
Q

Checkpoints of Glycolysis (3)

A
  1. Hexokinase/glucokinase
  2. PFK-1
  3. Pyruvate kinase
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13
Q

3 Checkpoint Enzymes Influenced by (4):

A

ATP, AMP, insulin, glucagon

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14
Q

Hexokinase

A

Present in all cells.
High affinity (even when Glc is low).
Inhibited by G6P.

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15
Q

Glucokinase

A

Present in liver and pancreatic beta cells.
Low affinity for Glc.
Not inhibited by G6P.
At low [Glc], translocates to nucleus.

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16
Q

PFK-1

A 
RLS.
\+ AMP, F 2,6-BP
- ATP, citrate
Active: Dephosphorylated
Inactive: Phosphorylated
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17
Q

Hormonal Regulation of PFK-1 (2)

A

+ Insulin, - Glucagon

  1. When insulin is high: dephosphorylates FBPase-2 produces F 2,6-BP, which activated PFK-1.
  2. When insulin is low (glucagon is high): Induces cAMP, phosphorylates PFK-2, reduces PFK-1 activity.
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18
Q

PK Function

A

Catalyzes conversion of PEP to pyruvate and ATP.

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19
Q

Regulation of PK

A

+ by F 1,6-BP and insulin
- by ATP, Alanine, and Glucagon
High insulin: activates PK
Low insulin: deactivates PK

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20
Q

Fates of G6P (1) and conversion to G1P (3) in Other Pathways

A

G6P: PPP
G1P: Gal. metabolism, glycogen synthesis, uronic acid pathway

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21
Q

Fates of G6P in Essential Metabolism (4)

A

Glc, Pyruvate, Glycogen, Ribose/NADPH

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22
Q

Fates of Pyruvate (4)

A
  1. Reduced to lactate (regen. NAD+)
  2. Oxidized in TCA
  3. Converted to Ala (GNG and PS)
  4. Ethanol (anaerobic conditions)
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23
Q

Ineffective Glycolysis (3)

A

Impacts cells that do not have mitochondria mostly (RBCs)
Most defects cause hemolytic anemias
PK is mostly affected enzyme

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24
Q

The Brain and Glc (3)

A

Only Glc can cross BBB.
When starved, brain uses Glc from the liver via GNG.
Can also use ketone bodies (extreme starvation or ketogenic diet) to create b-hydroxybutyrate.

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25
Q

Type 1 Diabetes

A

Insulin deficiency due to loss of pancreatic beta cells.

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26
Q

Type 2 Diabetes

A

Insulin resistance that progresses to loss of beta cell function.

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27
Q

Tarui Disease (GSD VII) (6)

A
  1. Deficient in PFK-1
  2. Least common GSD
  3. Exercised-induced muscle cramps/weakness
  4. Hemolytic anemia
  5. High bilirubin and jaundice
  6. Sx are usually mild
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28
Q

Glucose Stats (1. whole body 2. brain daily 3. present in body fluid 3. from glycogen)

A
  1. 160 g
  2. 120 g
  3. 20 g
  4. 190 g
    Direct Glc reserves sufficient for about 1 day.
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29
Q

Locations of Gluconeogenesis (GNG)

A

Liver, kidney, SI.

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30
Q

Major Precursors for GNG (aside from pyruvate)

A

Glycerol, Propionate, Alanine, AAs (minus Leu and Lys)

31
Q

Unique Enzymes for GNG (4)

A
  1. Pyruvate carboxykinase
  2. PEP Carboxylase
  3. F 1,6-BPhosphatase
  4. G 6-Phosphatase
32
Q

Enzymes from Glycolysis NOT found in GNG (3)

A
  1. Hexokinase/glucokinase
  2. PFK-1
  3. Pyruvate kinase
33
Q

Negative Regulators for Glycolysis (6)

A
  1. Glucagon
  2. ATP
  3. Citrate
  4. G 6-P
  5. F 6-P
  6. Alanine
34
Q

Positive Regulators for GNG (5)

A
  1. Glucagon
  2. Citrate
  3. Cortisol
  4. Thyroxine
  5. Acetyl CoA
35
Q

Negative Regulators for GNG (3)

A
  1. ADP
  2. AMP
  3. F 2,6-BP
36
Q

Pyruvate Carboxylase (PC)

A

Mitochondrial enzyme that converts pyruvate to OAA.

Biotin is a cofactor.

37
Q

Malate Dehydrogenase

A

Reduces OAA to malate so it can leave the mitochondria. Malate is reoxidized to OAA in cytosol by cytosolic malate DH.

38
Q

Rate Limiting Step of GNG

A

Fructose 1,6-BP

39
Q

Cori Cycle

A

Links lactate from anaerobic glycolysis in RBC and exercising muscle to GNG in the liver.

40
Q

F 1,6-BP Deficiency

A

D/O of GNG.
Similar to Tarui disease.
Presents in infancy or early childhood.

41
Q

Von Gierke Disease

A

Deficiency in G6P.

Unable to release Glc into blood by the liver in GNG and glycolysis.

42
Q

Fanconi-Bickel Syndrome

A

Mutation in GLUT 2 transporter.
Unable to take up Glc, Fru, and Gal.
Unable to thrive, hepatomegaly, abdominal bloating, rickets.

43
Q

Conversion of Glc to Fru-Polyol Pathway

A

Glc reduced to sorbitol by aldose reductase.
Sorbitol oxidized to Fru by Sorbitol DH.
Cells that do not have S DH can swell. Manifests as cataracts, mainly.

44
Q

HFCS and Obesity

A

Fru has lower glycemic index than sucrose, BUT is converted easily to fat as it bypasses he rate limiting step of PFK-1.

45
Q

Types of Galactosemia (2)

A
  1. GALT Deficiency: leads to accumulation of galactitol.

2. Deficiency in Galactokinase: leads to accumulation of Gal and galactitol, causing cataracts early in life.

46
Q

Overview of PPP

A

Occurs in cytosol.
Oxidizes G6P ro Ribulose 5-P.
Reduces NADP+ to NADPH (2x)
Produces 1 CO2

47
Q

Oxidative Phase of PPP (2)

A
  1. G6P DH: RLS. Creates 1 NADPH.

2. NADPH regenrates glutathione (important antioxidant that detoxifies H2O2)

48
Q

G6PD Deficiency

A

Affects ability to produce NADPH.
Higher incidence in African descent pts.
Presents as hemolytic anemia.

49
Q

Non-oxidative Phase of PPP

A

Reversible reactions.

Regenerates Glyceraldehyde 3-P. Shunts product to other pathways (glycolysis, GNG or nucleotide synthesis).

50
Q

Enzymes in Non-ox Phase of PPP (2)

A

Transketolase and Transaldolase

51
Q

Which Cells Have a High Demand for Ribose 5P?

A

Rapidly dividing cells (needs 5Cs for DNA synthesis

52
Q

Cells with High Activity of PPP (need NADPH)

A

Lung, liver, phagocytes.

53
Q

Non-reducing end of Glycogen

A

Glc molecule with a free -OH at C4 (terminal Glc).

54
Q

Glycogenin

A

Protein within glycogen that is connected to the reducing end.

55
Q

Glycogen Storage

A

Stored in liver and muscle mostly as granules.

Granules contain all that is needed for glycogen metabolism.

56
Q

Liver Glycogen

A

Regulates blood Glc levels.

57
Q

Muscle Glycogen

A

Reservoir for Glc for physical activity.

58
Q

3 Key Steps of Glycogenesis

A
  1. Trapping and Activation of Glc
  2. Elongation of glycogen primer
  3. Branching of gycogen
59
Q

Trapping and Activation of Glc (3)

A
  1. Hexo/gluco convert Glc to G6P which traps Glc in cell.
  2. Phosphoglucomutase reversibly isomerizes G6P to G1P.
  3. UDP-glucose pyrophosphorylase transfers G1P to UTP and creates UDP-glucose
60
Q

Elongation of Glycogen Primer (1)

A

Glycogen synthase (RL enzyme) catalyzes transfer of UDP-glucose to non-reducing end.

61
Q

Branching of Glycogen (1)

A

Glucosyl (4:6) transferase transfers glycogen chains (after about 11 residues (it takes about 7 residues and reattaches elsewhere).

62
Q

2 Key Steps of Glycogenolysis

A
  1. Chain shortening

2. Branch transfer and release of Glc

63
Q

Chain Shortening (3)

A
  1. Glycogen phoshorylase (RL enzyme) cleaves at non-reducing end.
  2. Pyridoxal phosphate (Vit B6) is a cofactor.
  3. Process continues until GP is within 4 residues of an a-1,6 branch point linkage.
64
Q

Branch Transfer and Release of Glc (2)

A
  1. Debranching enzyme transfers a block of 3 of the 4 remaining Glc to non-reducing end.
  2. Enzymes then cleave the a-1,6 bond of the 1 remaining Glc residue.
65
Q

Fate of Liver G1P

A

G1P converted to G6P and then to Glc by G6Phosphatase and released into blood.

66
Q

Fate of Muscle G1P

A

G6P used to make energy in glycolysis and TCA cycle.

67
Q

2 Key Enzymes for Glycogen Metabolism

A

Glycogen synthase: RLS of synthesis
Glycogen phosphorylase: RLS of degredation
BOTH regulated by phophorylation

68
Q

When is Glycogen Synthase Active?

A

Dephophorylation: active
Phosphorylated: inactive

69
Q

When is Glycogen Phosphorylase Active?

A

Dephophorylation: inactive
Phosphorylated: active

70
Q

GSD 0

A

Defective enzyme: glycogen synthase

Pathway affected: chain elongation

71
Q

GSD II (Pompe Disease)

A

Defective enzyme: Acid maltase

Pathway affected: Lysosomal glycogenolysis (release of Glc)

72
Q

GSD IV (Andersen Disease)

A

Defective enzyme: Glucosyl (4:6) transferase

Pathway affected: chain branching

73
Q

GSD V (McArdle Disease)

A

Defective enzyme: Muscle glycogen phosphorylase

Pathway affected: Glycogenolysis (G1P release)

74
Q

GSP VI (Hers Disease)

A

Defective enzyme: Liver glycogen phosphorylase

Pathway affected: Glycogenolysis (G1P release)

MCM Exam 1 (10 decks)

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