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MCM Exam 1 > Lect 4 CHO Metabolism > Flashcards

Lect 4 CHO Metabolism Flashcards

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
Q

Failure of glycolysis results in _ leading to disruption of ion gradients.

This causes what to happen and what condition?

A

ATP Deficiency –> Reduced cell viability

RBC destruction causes hemolytic anemia

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26
Q

Why is the brain particularly dependent on glucose?

What happens during starvation?

A

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)

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27
Q

Diabetes is characterized by _

Differences between Type I and Type II

Fasting glucose levels in prediabetic and diabetic

A
  • 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
Q

How much Glucose does the body need? the brain?

How much is availabel in body fluids? glycogen stores?

A

Needs 160 g glucose/day

Brain requires 120 g

Glucose in body fluids 20 g

Glucose available from glycogen 190 g

29
Q

Gluconeogenesis Location, Function, Precursors

A

Location: Liver, Kidney, SI

Function: Pyruvate –> Glucose

Precursors: Lactate, AAs, Glycerol

30
Q

What is Pyruvate Carboxylase (PC)

A
  • Mitochondrial Enzyme that catalyzes 1st Step:
    • Pyruvate carboxylated to form OAA
31
Q

Pyruvate Carboxylase cofactor?

32
Q

Pyruvate Carboxylase Regulation

A

Activated: Acetyl CoA and Cortisol

Inhibited: ADP

33
Q

How is Pyruvate transported out of Mitochondria

A
  • 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
Q

What is the function of Phosphoenolpyruvate Carboxykinase (PEPCK)

A

OAA –> PEP

Activated: Cortisol, Glucagon, Thyroxine

35
Q

Fructose 1,6-Bisphosphatase

A

F1,6-BP –> F6P

Rate Limiting Step

Activated: Cortisol and Citrate

Inhibited: AMP and F26BP

36
Q

What does Glucose 6 Phosphatase do?

A

G6P –> Glucose

Activated by Cortisol

37
Q

Glucose 6 Phosphatase Location and Structure

A

Lumen of ER in Liver, Kidneys, SI, and Pancreas

Catalytic Unit; G6P/Pi antiporter; glucose transporter (GLUT7)

38
Q

What is the Function of Cori Cycle?

A

Lactate from anaerobic glycolysis in RBC/exercising muscle –> Liver (gluconeogenesis)

39
Q

F1,6-Bisphosphatase Deficiency Consequences

A

Hypoglycemia, lactic acidosis, ketosis, apnea, hyperventilation

40
Q

What is Von Gierke Disease (GSD1a)?

A

Deficiency in glucose 6 phosphatase

41
Q

Fructose Uptake Transporter?

A

GLUT5 (Facilitated Diffusion)

42
Q

Galactose/Glucose Uptake Transporter?

A

SGLT1 (Secondary Active Transport w/ Na)

43
Q

Fanconi Bickel Syndrome Cause and Defects

A

Mutation in GLUT2 transporter (liver, pancreatic B cell, enterocytes, renal tubular cells)

Unable to uptake Glu, Fru, Gal

44
Q

Conversion of Glucose to Fructose via Polyol Pathway

A

Glucose –> Sorbitol (Aldose reductase) –> Fructose (Sorbitol dehydrogenase)

Cells lacking sorbitol dehydrogenase (kidney, retina) accumulate sorbitol (water influx/swelling) and manifest as retinopathy, cataracts

45
Q

High Fructose Corn Syrup (HCFS) and Obesity

A

Bypasses PFK-1, more efficiently converted to Fat

46
Q

How is Galactose Metabolism

A

Galactose –> Galactose 1P (galactokinase) –> Glucose 1P (Glucose 1P Uridyltransferase/GALT) <– RLS

47
Q

Galactosemia is caused by what?

A
  • Deficiency in GALT
  • Deficiency in Galactokinase
48
Q

PPP Location and Products

A

Occurs in cytosol

Oxidation of G6P –> Ribulose 5P

Reduction of NADP+ –> NADPH (2)

49
Q

Irreversible Oxidative Step (Catabolism)

A

G6P –> 6PLactone (G6P Dehydrogenase) –> 6PGluconate –> Ribulose 5P

Produces 2 NADPH

G6PDH Inhibited by NADPH

50
Q

PPP Rate Limiting Enzyme

A

G6P Dehydrogenase

51
Q

NADPH regenerates _

A

Glutathione (antioxidant, detoxifies H2O2)

52
Q

PPP - Nonoxidative phase is series of _ reactions.

These end products are shunted to glycolytic, gluconeogenic, and nucleotide synthesis pathways.

A

Reversible

Ribose 5P, G3P, F6P

53
Q

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

A

Oxidative - Ribulose 5P

Non - oxidative

54
Q

Glucose molecules are linked together via _ bonds in glycogen with branch points formed via _ bonds

A

a-1,4 glycosidic bonds

a-1,6 glycosidic bonds

55
Q

Glycogen stored in _ which contain not only glycogen but also _

A

Granules

Enzymes needed for glycogen metabolism

56
Q

Trapping and activation of glucose in glycogenesis in 3 steps

Occurs in liver and muscle

A
  • Glucose –> G6P
    • HK/GK
  • G6P –> G1P
    • Phosphoglucomutase
  • G1P –> UDP Glucose (Active Form)
    • UDP Glucose pyrophosphorylase
57
Q

Elongation of glycogen primer utilizes this rate limiting enzyme

A

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

58
Q

Branching of glycogen chains occurs via this enzyme

Why is branching important?

A

Glucosyl (4:6) transferase

Increases solubility of glycogen and increases number of non-reducing terminal ends

59
Q

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

A

Glycogen phosphorylase

Pyridoxal phosphate (Vit B6)

4 residues

60
Q

This enzyme transfers block of 3 of 4 remaining glucose to non reducing end.

A

Debranching enzyme

61
Q

In the liver, G1P is converted to G6P and then to glucose by this enzyme that is not present in muscles

A

Phosphatase

62
Q

GP and GS are regulated by phosphorylation.

GS is active when _

GP is active when _

A

GS: active dephosphorylated/inactive phosphorylated

GP: active phosphorylated/inactive dephosphorylated

63
Q

Reciprocal regulation of glycogenesis and glycogenolysis

64
Q

Insulin regulation mechanism has 4 key proteins involved and what is the net result?

A
  • GLUT4, Protein Kinase B, Protein Phosphatase 1, Glycogen Synthase Kinase 3
  • Net Result Glycogen Synthesis
65
Q

Regulation of Glycogenolysis has 5 key enzymes and second messengers

A
  • G protein, Adenylate cyclase (AC) and cAMP, PKA, PP1, Phosphorylase Kinase
  • Net result is glycogen breakdown
66
Q

GSD 0

GSD II/Pompe Disease

GSD III/Cori Disease

GSD IV/Anderson Disease

GSD V/McArdle Disease

GSD VI/Hers Disease

A
  • 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

MCM Exam 1 (11 decks)

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