Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

GLUT 2

A

Main transporter in liver.

Low affinity for Glc. (Unreg.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

GLUT 3

A

Main transporter in neurons.

High affinity for Glc. (Unreg.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

GLUT 4

A

Present in skeletal muscle, heart and adipose tissue.

Insulin dependent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

More on GLUT 4:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 Phases of Glycolysis

A
  1. Investment
  2. Splitting
  3. Payoff
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Net Yield of Glycolysis

A

2 ATP, 2 NADH, 2 pyruvate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Splitting Phase (2)

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

5. Isomerization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Checkpoints of Glycolysis (3)

A
  1. Hexokinase/glucokinase
  2. PFK-1
  3. Pyruvate kinase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

3 Checkpoint Enzymes Influenced by (4):

A

ATP, AMP, insulin, glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hexokinase

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PFK-1

A 
RLS.
\+ AMP, F 2,6-BP
- ATP, citrate
Active: Dephosphorylated
Inactive: Phosphorylated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

PK Function

A

Catalyzes conversion of PEP to pyruvate and ATP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Fates of G6P in Essential Metabolism (4)

A

Glc, Pyruvate, Glycogen, Ribose/NADPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Type 1 Diabetes
Insulin deficiency due to loss of pancreatic beta cells.
26
Type 2 Diabetes
Insulin resistance that progresses to loss of beta cell function.
27
Tarui Disease (GSD VII) (6)
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
28
Glucose Stats (1. whole body 2. brain daily 3. present in body fluid 3. from glycogen)
1. 160 g 2. 120 g 3. 20 g 4. 190 g Direct Glc reserves sufficient for about 1 day.
29
Locations of Gluconeogenesis (GNG)
Liver, kidney, SI.
30
Major Precursors for GNG (aside from pyruvate)
Glycerol, Propionate, Alanine, AAs (minus Leu and Lys)
31
Unique Enzymes for GNG (4)
1. Pyruvate carboxykinase 2. PEP Carboxylase 3. F 1,6-BPhosphatase 4. G 6-Phosphatase
32
Enzymes from Glycolysis NOT found in GNG (3)
1. Hexokinase/glucokinase 2. PFK-1 3. Pyruvate kinase
33
Negative Regulators for Glycolysis (6)
1. Glucagon 2. ATP 3. Citrate 4. G 6-P 5. F 6-P 6. Alanine
34
Positive Regulators for GNG (5)
1. Glucagon 2. Citrate 3. Cortisol 4. Thyroxine 5. Acetyl CoA
35
Negative Regulators for GNG (3)
1. ADP 2. AMP 3. F 2,6-BP
36
Pyruvate Carboxylase (PC)
Mitochondrial enzyme that converts pyruvate to OAA. | Biotin is a cofactor.
37
Malate Dehydrogenase
Reduces OAA to malate so it can leave the mitochondria. Malate is reoxidized to OAA in cytosol by cytosolic malate DH.
38
Rate Limiting Step of GNG
Fructose 1,6-BP
39
Cori Cycle
Links lactate from anaerobic glycolysis in RBC and exercising muscle to GNG in the liver.
40
F 1,6-BP Deficiency
D/O of GNG. Similar to Tarui disease. Presents in infancy or early childhood.
41
Von Gierke Disease
Deficiency in G6P. | Unable to release Glc into blood by the liver in GNG and glycolysis.
42
Fanconi-Bickel Syndrome
Mutation in GLUT 2 transporter. Unable to take up Glc, Fru, and Gal. Unable to thrive, hepatomegaly, abdominal bloating, rickets.
43
Conversion of Glc to Fru-Polyol Pathway
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
HFCS and Obesity
Fru has lower glycemic index than sucrose, BUT is converted easily to fat as it bypasses he rate limiting step of PFK-1.
45
Types of Galactosemia (2)
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
Overview of PPP
Occurs in cytosol. Oxidizes G6P ro Ribulose 5-P. Reduces NADP+ to NADPH (2x) Produces 1 CO2
47
Oxidative Phase of PPP (2)
1. G6P DH: RLS. Creates 1 NADPH. | 2. NADPH regenrates glutathione (important antioxidant that detoxifies H2O2)
48
G6PD Deficiency
Affects ability to produce NADPH. Higher incidence in African descent pts. Presents as hemolytic anemia.
49
Non-oxidative Phase of PPP
Reversible reactions. | Regenerates Glyceraldehyde 3-P. Shunts product to other pathways (glycolysis, GNG or nucleotide synthesis).
50
Enzymes in Non-ox Phase of PPP (2)
Transketolase and Transaldolase
51
Which Cells Have a High Demand for Ribose 5P?
Rapidly dividing cells (needs 5Cs for DNA synthesis
52
Cells with High Activity of PPP (need NADPH)
Lung, liver, phagocytes.
53
Non-reducing end of Glycogen
Glc molecule with a free -OH at C4 (terminal Glc).
54
Glycogenin
Protein within glycogen that is connected to the reducing end.
55
Glycogen Storage
Stored in liver and muscle mostly as granules. | Granules contain all that is needed for glycogen metabolism.
56
Liver Glycogen
Regulates blood Glc levels.
57
Muscle Glycogen
Reservoir for Glc for physical activity.
58
3 Key Steps of Glycogenesis
1. Trapping and Activation of Glc 2. Elongation of glycogen primer 3. Branching of gycogen
59
Trapping and Activation of Glc (3)
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
Elongation of Glycogen Primer (1)
Glycogen synthase (RL enzyme) catalyzes transfer of UDP-glucose to non-reducing end.
61
Branching of Glycogen (1)
Glucosyl (4:6) transferase transfers glycogen chains (after about 11 residues (it takes about 7 residues and reattaches elsewhere).
62
2 Key Steps of Glycogenolysis
1. Chain shortening | 2. Branch transfer and release of Glc
63
Chain Shortening (3)
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
Branch Transfer and Release of Glc (2)
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
Fate of Liver G1P
G1P converted to G6P and then to Glc by G6Phosphatase and released into blood.
66
Fate of Muscle G1P
G6P used to make energy in glycolysis and TCA cycle.
67
2 Key Enzymes for Glycogen Metabolism
Glycogen synthase: RLS of synthesis Glycogen phosphorylase: RLS of degredation BOTH regulated by phophorylation
68
When is Glycogen Synthase Active?
Dephophorylation: active Phosphorylated: inactive
69
When is Glycogen Phosphorylase Active?
Dephophorylation: inactive Phosphorylated: active
70
GSD 0
Defective enzyme: glycogen synthase | Pathway affected: chain elongation
71
GSD II (Pompe Disease)
Defective enzyme: Acid maltase | Pathway affected: Lysosomal glycogenolysis (release of Glc)
72
GSD IV (Andersen Disease)
Defective enzyme: Glucosyl (4:6) transferase | Pathway affected: chain branching
73
GSD V (McArdle Disease)
Defective enzyme: Muscle glycogen phosphorylase | Pathway affected: Glycogenolysis (G1P release)
74
GSP VI (Hers Disease)
Defective enzyme: Liver glycogen phosphorylase | Pathway affected: Glycogenolysis (G1P release)

MCM Exam 1 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions