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MCM Exam 1 > Lect 4 CHO Metabolism > Flashcards

Lect 4 CHO Metabolism Flashcards

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1
Q

What is the only fuel RBCs can use?

A

Glucose (no mitochondria)

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2
Q

What energy forms does the Brain use?

A

Glucose (non-starvation)

Switch to Ketones (starvation)

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3
Q

Where is GLUT1?

A

Ubiquitous, but high in RBC and brain

High affinity Km 1 mM

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4
Q

Where is GLUT2?

A

Main transporter in Liver

Low Affinity Km 10 mM

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5
Q

Where is GLUT3?

A

Main transporter in neurons

High Affinity Km 1 mM

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6
Q

Where is GLUT4?

A

Skeletal muscle, heart, adipose tissue

Regulated: Insulin Dependent

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7
Q

How is GLUT4 brought to the plasma membrane?

A

GLUT4 sequestered in vesicles in cells

Insulin signaling –> fusion of vesicles with PM

Enables GLUT4 induced glucose uptake

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8
Q

Glycolysis is _ process

A

Anaerobic (no O2)

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9
Q

Where does Glycolysis occur?

A

Cytoplasm

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10
Q

What is Glycolysis’s Net Yield

A

2 ATP

2 NADH

2 Pyruvate

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11
Q

Describe Glycolysis Phase 1 (Investment Phase)

A
  • Phosphorylation of Glucose –> G6P (Regulatory Step)
    • Hexokinase (all cells) & Glucokinase (liver, pancreatic B-cells)
      • ATP –> ADP
  • Isomerization of G6P to F6P
  • Phosphorylation of F6P –> Fructose 1,6-Bisphosphate (F1,6-BP) (RATE LIMITING STEP​)
    • Phosphofructokinase-1 (PFK-1)
      • ​ATP –> ADP
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12
Q

How is Hexokinase Regulated?

What is its affinity?

A

Inhibited by G6P

High Affinity (functional even at low [glucose])

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13
Q

How is Glucokinase Regulated?

What is its affinity?

A

Activated: Glucose, F1P, Insulin

Inhibited: Glucagon, F6P

Low affinity for glucose

Most active when high [glucose]

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14
Q

How is PFK-1 Regulated?

A

Activate: AMP, F2,6-BP (formed by PFK-2)

Inhibit: ATP, Citrate

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15
Q

How is PFK-1 Hormonally Regulated with Insulin?

A
  • Fed State:
    • High insulin/low glucagon
    • Activate protein phosphatases, Dephosphorylate PFK-2/FBPase-2 (Kinase activity) produces F2,6BP –> activating PFK-1
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16
Q

How is PFK-1 Hormonally Regulated with Glucagon?

A
  • Fasting State
    • High glucagon/low insulin
    • Induces high [cAMP] –> activate PKA, phosphorylates PFK-2/FBPase-2 (phosphorylation activity) –> Reduces PFK-1 activity
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17
Q

Describe Glycolysis Phase 2 (Splitting)

A
  • Cleavage of F1,6-BP –> Dihydroxyacetone Phosphate (DHAP) + Glyceraldehyde 3P (G3P)
    • Aldolase A
  • Isomerization of DHAP –> G3P (Now have 2 G3P)
    • Triose Phosphate Isomerase
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18
Q

Describe Glycolysis Phase 3 (Payoff)

A
  • G3P (2) –> 1,3-Bisphosphoglycerate (2)
    • Glyceraldehyde 3P Dehydrogenase
      • Reduces NAD+ (2) –> NADH (2)
  • ​​1,3-BPG (2) –> 3-Phosphoglycerate (3PG) (2)
    • Phosphoglycerate Kinase
      • ADP (2) –> ATP (2)​
  • 3PG –> 2PG –> PEP
  • PEP (2) –> Pyruvate (2)
    • Pyruvate Kinase
      • ADP (2) –> ATP (2)
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19
Q

Describe Pyruvate Kinase Regulation

A
  • Activated: Insulin, F1,6-BP
  • Inhibit: Alanine, ATP, Glucagon
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20
Q

Describe PK Hormonal Regulation

A
  • High Insulin: Stimulate protein phosphotase –> Dephosphorylation of PK –> Activate
  • High Glucagon: cAMP activates PKA –> Phosphorylation of PK –> Inhibition
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21
Q

3 Regulation Checkpoints of Glycolysis

A

Hexokinase/Glucokinase (Glu –> G6P)

PFK-1 (F6P –> F16BP)

Pyruvate Kinase (PEP –> Pyruvate)

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22
Q

What are the other fates of G6P?

A
  • Pentose Phosphate Pathway: G6P –> Ribose and NADPH Synthesis
  • Converted to G1P: Gylcogen synthesis, Gal metabolism
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23
Q

Defective Glycolytic Enzymes = _

What cells most affected?

Most common enzyme defective?

A

Ineffective glycolysis

Cells w/o Mitochondria impacted most (RBC)

Pyruvate Kinase

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24
Q

Most Glycolytic Enzyme Defects cause this condition

A

Hemolytic Anemias

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25
Failure of glycolysis results in _ leading to disruption of ion gradients. This causes what to happen and what condition?
**ATP Deficiency** --\> Reduced cell viability RBC **destruction** causes **hemolytic anemia**
26
Why is the brain particularly dependent on glucose? What happens during starvation?
Glucose only fuel molecule to **cross blood brain barrier (BBB)** **Starvation:** obtain glucose from liver via gluconeogenesis Also utilize ketone bodies (extreme starvation/ketogenic diet)
27
Diabetes is characterized by \_ Differences between Type I and Type II Fasting glucose levels in prediabetic and diabetic
* Characterized by **hyperglycemia** * **Type I: insulin deficiency** due to **loss of pancreatic B-cells** * **Type II:** **insulin resistance** progresses to **loss of B-cell function** * Prediabetic = 100-125 * Diabetic = \> 125
28
How much Glucose does the body need? the brain? How much is availabel in body fluids? glycogen stores?
**Needs 160 g glucose/day** **Brain requires 120 g** **Glucose in body fluids 20 g** **Glucose available from glycogen 190 g**
29
Gluconeogenesis Location, Function, Precursors
Location: **Liver, Kidney, SI** Function: **Pyruvate --\> Glucose** Precursors: **Lactate, AAs, Glycerol**
30
What is Pyruvate Carboxylase (PC)
* **Mitochondrial Enzyme** that catalyzes 1st Step: * **Pyruvate carboxylated to form OAA**
31
Pyruvate Carboxylase cofactor?
Biotin
32
Pyruvate Carboxylase Regulation
Activated: **Acetyl CoA and Cortisol** Inhibited: **ADP**
33
How is Pyruvate transported out of Mitochondria
* **OAA reduced --\> Malate via Malate Dehydrogenase (NADH dependent)** * Transported to cytoplasm via **Malate shuttle** * **Re-oxidized to OAA via cytosolic malate dehyrogenase (NADH dependent)**
34
What is the function of Phosphoenolpyruvate Carboxykinase (PEPCK)
**OAA --\> PEP** Activated: Cortisol, Glucagon, Thyroxine
35
Fructose 1,6-Bisphosphatase
**F1,6-BP --\> F6P** **Rate Limiting Step** Activated: Cortisol and Citrate Inhibited: AMP and F26BP
36
What does Glucose 6 Phosphatase do?
G6P --\> Glucose Activated by Cortisol
37
Glucose 6 Phosphatase Location and Structure
Lumen of ER in Liver, Kidneys, SI, and Pancreas Catalytic Unit; G6P/Pi antiporter; glucose transporter (GLUT7)
38
What is the Function of Cori Cycle?
**Lactate from anaerobic glycolysis in RBC/exercising muscle --\> Liver (gluconeogenesis)**
39
F1,6-Bisphosphatase Deficiency Consequences
Hypoglycemia, lactic acidosis, ketosis, apnea, hyperventilation
40
What is Von Gierke Disease (GSD1a)?
**Deficiency in glucose 6 phosphatase**
41
Fructose Uptake Transporter?
**GLUT5 (Facilitated Diffusion)**
42
Galactose/Glucose Uptake Transporter?
**SGLT1 (Secondary Active Transport w/ Na)**
43
Fanconi Bickel Syndrome Cause and Defects
**Mutation in GLUT2 transporter** (liver, pancreatic B cell, enterocytes, renal tubular cells) ## Footnote **Unable to uptake Glu, Fru, Gal**
44
Conversion of Glucose to Fructose via Polyol Pathway
Glucose --\> **Sorbitol (Aldose reductase)** --\> **Fructose (Sorbitol dehydrogenase)** Cells lacking **sorbitol dehydrogenase** (kidney, retina) accumulate sorbitol (water influx/swelling) and manifest as retinopathy, **cataracts**
45
High Fructose Corn Syrup (HCFS) and Obesity
Bypasses PFK-1, more efficiently converted to Fat
46
How is Galactose Metabolism
Galactose --\> Galactose 1P (galactokinase) --\> Glucose 1P (**Glucose 1P Uridyltransferase/GALT) \<-- RLS**
47
Galactosemia is caused by what?
* **Deficiency in GALT** * **Deficiency in Galactokinase**
48
PPP Location and Products
Occurs in **cytosol** Oxidation of G6P --\> **Ribulose 5P** Reduction of NADP+ --\> **NADPH (2)**
49
Irreversible Oxidative Step (Catabolism)
G6P --\> 6PLactone (**G6P Dehydrogenase)** --\> 6PGluconate --\> **Ribulose 5P** ## Footnote **Produces 2 NADPH** **G6PDH Inhibited by NADPH**
50
PPP Rate Limiting Enzyme
G6P Dehydrogenase
51
NADPH regenerates \_
**Glutathione** (antioxidant, detoxifies H2O2)
52
PPP - Nonoxidative phase is series of _ reactions. These end products are shunted to glycolytic, gluconeogenic, and nucleotide synthesis pathways.
**Reversible** **Ribose 5P, G3P, F6P**
53
Where there is a high demand of ribose 5P (nucleotide syn), _ phase is favored to produce \_ When there is high demand for NADPH, _ phase products channeled into gluconeogenesis for re-entry into PPP
Oxidative - Ribulose 5P Non - oxidative
54
Glucose molecules are linked together via _ bonds in glycogen with branch points formed via _ bonds
a-1,4 glycosidic bonds a-1,6 glycosidic bonds
55
Glycogen stored in _ which contain not only glycogen but also \_
Granules Enzymes needed for glycogen metabolism
56
Trapping and activation of glucose in glycogenesis in 3 steps Occurs in liver and muscle
* **Glucose --\> G6P** * **HK/GK** * **G6P --\> G1P** * **Phosphoglucomutase** * **G1P --\> UDP Glucose (Active Form)** * **UDP Glucose pyrophosphorylase**
57
Elongation of glycogen primer utilizes this rate limiting enzyme
Glycogen synthase catalyzes transfer of glucose from UDP-glucose to non-reducing end of glycogen
58
Branching of glycogen chains occurs via this enzyme Why is branching important?
Glucosyl (4:6) transferase Increases solubility of glycogen and increases number of non-reducing terminal ends
59
Glycogenolysis starts with chain shortening phase to release G1P via this rate limiting enzyme What cofactor is used? Process continues until enzyme gets within _ residues of a-1,6 linkage
Glycogen phosphorylase Pyridoxal phosphate (Vit B6) 4 residues
60
This enzyme transfers block of 3 of 4 remaining glucose to non reducing end.
Debranching enzyme
61
In the liver, G1P is converted to G6P and then to glucose by this enzyme that is not present in muscles
Phosphatase
62
GP and GS are regulated by phosphorylation. GS is active when \_ GP is active when \_
GS: active dephosphorylated/inactive phosphorylated GP: active phosphorylated/inactive dephosphorylated
63
Reciprocal regulation of glycogenesis and glycogenolysis
64
Insulin regulation mechanism has 4 key proteins involved and what is the net result?
* **GLUT4, Protein Kinase B, Protein Phosphatase 1, Glycogen Synthase Kinase 3** * **Net Result Glycogen Synthesis**
65
Regulation of Glycogenolysis has 5 key enzymes and second messengers
* G protein, Adenylate cyclase (AC) and cAMP, PKA, PP1, Phosphorylase Kinase * Net result is glycogen breakdown
66
GSD 0 GSD II/Pompe Disease GSD III/Cori Disease GSD IV/Anderson Disease GSD V/McArdle Disease GSD VI/Hers Disease
* Deficiency in GS * Chain elongation * Deficiency in acid maltase (a-glucosidase) * Lysosomal glycogenolysis * Deficiency in a-1,6 glucosidase (Debranching Enzyme) * Glycogen molecules with large number of short branches * Deficiency in glucosyl (4:6) transferase (Branching Enzyme) * Long chain glycogen with fewer branches * Deficiency in muscle glycogen phosphorylase * Cannot supply muscles with glucose * Deficiency in Liver glycogen phosphorylase * Glycogen accumulates in liver, hypoglycemia

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