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Exam 1 > Carbohydrate Metabolism > Flashcards

Carbohydrate Metabolism Flashcards

1
Q

What is the starting molecule of glycolysis, and what are the end products?

A
  • 1 molecule of glucose

- 2 molecules of pyruvate and 2 molecules of ATP

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2
Q

What kind of cells are powered solely by glycolysis?

A
  • Red Blood Cells
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3
Q

Why can’t glucose enter the cell on its own?

A
  • Polarity of glucose
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4
Q

What kind of transporters move glucose into the cell?

A
  • GLUT transporters
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5
Q

What are the 4 types of GLUT transporters, and where are they located?

A
  • GLUT1: ubiquitous. High in RBCs and brain.
  • GLUT2: Main transporter in liver.
  • GLUT3: main transporter in neurons
  • GLUT4: present in skeletal muscle, heart, and adipose tissue
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6
Q

Which GLUT receptor is insulin dependent?

A

GLUT4

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7
Q

Where does Glycolysis occur?

A

Cytoplasm

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8
Q

What are the three phases of glycolysis?

What is consumed/generated in each step?

A
  • Investment: requires 2 ATP
  • Splitting: Generates 2 3-carbon molecules
  • Recoup: 4 ATP molecules are generated
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9
Q

What are the enzymes that initiate glycolysis? Where are they found?

A
  • Hexokinase: All Cells

- Glucokinase: Liver Cells

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10
Q

What is the rate limiting step of glycolysis?

A

Conversion of Fructose 6-P to Fructose 1,6-BP

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11
Q

What is the rate limiting enzyme for glycolysis?

A

Phosphofructokinase-1

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12
Q

What are the 3 steps of the investment phase of glycolysis?

A
  1. Phosphorylation of Glucose to G6P (traps glucose in cell)
  2. Isomerization of G6P to F6P
  3. Phosphorylation of F6P to F-1,6-BP (rate limiting)
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13
Q

What are the two steps of the splitting phase of glycolysis? What enzymes are used?

A
  1. Cleavage of F-1,6-BP to DHAP and G3P via ALDOSE A

2. Isomerization of these two products via triose phosphate isomerase.

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14
Q

What are the 3 steps of the payoff phase of glycolysis? What enzymes are used, and where are products formed?

A
  1. Phosphorylation of G3P to 1,3-BPG
    - uses GADPH, makes 2 NADH
  2. Conversion of 1,3-BPG to 3-PG
    - Uses phosphoglycerate kinase, makes 2 ATP
  3. Formation of pyruvate
    - uses Pyruvate Kinase, makes 2 ATP
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15
Q

What enzyme catalyzes the step where the first ATP is made in glycolysis?

A

Phosphoglycerate kinase

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16
Q

What are the enzymes used in the three irreversible phosphorylation steps in glycolysis?

A
  1. Hexokinase/glucokinase
  2. Phosphofructokinase-1
  3. Pyruvate Kinase
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17
Q

What are the two main differences between hexokinase and glucokinase?

A
  1. Hexokinase is in all cells, glucokinase is only in the liver
  2. Hexokinase can use other sugars as its substrate
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18
Q

Hexokinase is inhibited by______

A

G6P (product)

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19
Q

The rate limiting enzyme in glycolysis is ______

A

PFK-1

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20
Q

PFK-1 is activated by (1) and is inhibited by (2)

A
  1. AMP, Fructose-2,6-BP

2. ATP, Citrate

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21
Q

____ is the hormone that stimulates PFK-1, and ____ is the hormone that inhibits PFK-1.

A
  1. Insulin

2. Glucagon

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22
Q

What is tarui disease? What is it a deficiency of?

A
  • Deficiency of PFK-1

- symptoms can be mild, induced muscle cramps and soreness.

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23
Q

Pyruvate Kinase catalyzes the reaction of ____ into ____

A

Phosphoenol Pyruvate (PEP) into Pyruvate and ATP

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24
Q

Pyruvate Kinase is activated by (1) and inactivated by (2)

A
  1. F-1,6-BP & insulin

2. ATP, Alanine, Glucagon

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25
Q

Which Glycolysis intermediate is used as the precursor for the pentose-5-phosphate pathway?

A
  • Glucose-6-phosphate
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26
Q

Which cells are affected the most by defects in glycolysis?

27
Q

What is the result of pyruvate kinase deficiency

A
  • hemolytic anemia, caused by erythrocyte mutation
28
Q

In the ____ state glucose is abundant, there is inceased uptake, increased rates of glycolyis, production of glycogen, and decreased gluconeogenesis.

29
Q

In the _____ state there is low glucose, decreased uptake, less storage, increase in gluconeogenesis, and glycogenolysis.

A

Fasting state.

30
Q

What is the difference between type 1 and type 2 diabetes?

A

Type 1 = loss of pancreatic beta cells

Type 2 = insulin resistance leads to loss of Beta cell function

31
Q

What is fanconi bickel syndrome? What is its pattern of inheritance?

A
  1. Mutation in GLUT2 transporter
  2. Unable to take up glucose, fructose, and galactose
  3. Treat with vitamin D and phosphate
  4. Autosomal recessive disorder
32
Q

How much daily glucose does your brain, and body need to function?

A
  • brain = 120g a day

- body = 160g a day

33
Q

What is gluconeogenesis?

A
  • synthesis of glucose from carbohydrate and non-carbohydrate precursors.
34
Q

What gluconeogenesis enzymes are equivalent (comparable) to those used in glycolysis ( Hexo/glucokinase, PFK-1, and Pyruvate Kinase).

A
  1. Hexo/glucokinase = Glucose-6-phosphatase
  2. PFK-1 = fructose-1,6-bisphosphatase
  3. Pyruvate Kinase = PEP Carboxykinase + pyruvate carboxylase
35
Q

What are the major 6 rxns of gluconeogenesis and what are their enzymes?

A
  1. Pyruvate to OAA via pyruvate carboxylase
  2. OAA to PEP via PEP carboxykinase
  3. PEP to Fructose-1,6-bisphosphate
  4. F1,6BP to F6P via Fructose-1,6-bisphosphatase
  5. F6P to G6P
  6. G6P to Glucose via Glucose 6 phosphatase
36
Q

What is the rate limiting enzyme of gluconeogenesis?

A

Fructose-1,6-bisphosphatase

37
Q

What is the first enzyme in Gluconeogenesis?

A

Pyruvate carboxylase

38
Q

What does pyruvate carboxylase catalyze?

A

Conversion of pyruvate to OAA

39
Q

What is pyruvate carboxylases cofactor?

A

Biotin (B7)

40
Q

Oxaloacetate has to leave mitochondria to participate in Gluconeogenesis, how does this occur?

A

OAA is converted to malate by Mitochondrial Malate Dehydrogenase, moved out of mitochondria via Malate Shuttle, and is converted back to OAA by Cytosolic malate dehydrogenase.

41
Q

What regulates the conversion of OAA to PEP?

A

PEPCK (phosphoenolpyruvate carboxykinase)

42
Q

What breaks down Fructose-1,6-bisphosphate to F6P?

A

Fructose-1,6-bisphosphatase

—> this is the rate limiting enzyme/ step

43
Q

Where is glucose 6 phosphatase found? What does it do?

A

Liver, kidneys, small intestine. It converts G6P to Glucose

44
Q

What is the Cori cycle?

A
  • Takes lactate produced by anaerobic glycolysis in RBC and exercising muscle to liver to regenerate glucose.
45
Q

Before entering gluconeogenesis, galactose and glycogen must convert to (1) before entering gluconeogenesis as (2)

A
  1. Glucose-1-phosphate

2. Glucose-6-phosphate

46
Q

What intermediate form does glycerol have to take before entering gluconeogenesis?

A

Glycerol-3-phosphate to DHAP

47
Q

What intermediate form do lactate and alanine have to take before entering gluconeogenesis?

48
Q

What is Fructose-1,6-bisphosphatase deficiency, what are its symptoms.

A
  • similar to tarui disease

- leads to chronic hypoglycemia and lactic acidosis

49
Q

What is Von Gierke Disease(called GSD1 also)?

A

Deficiency in glucose-6-phosphatase. Ineficient release of free glucose into the blood stream by the liver. Dietary management is treatment.

50
Q

Conversion of Glucose into Fructose -

Glucose is reduced to (1) by (2)

A
  1. Sorbitol

2. Aldose reductase

51
Q

Conversion of glucose to fructose -

Sorbitol is oxidized to (1) by (2)

A
  1. Fructose

2. Sorbitol dehydrogenase

52
Q

Describe Sorbitol accumulation

A

Cells that lack sorbitol dehydrogenase can accumulate sorbitol. This can manifest as cataracts or retinopathy.

53
Q

Describe Fructose Metabolism

A
  1. Fructose can enter glycolysis as Fructose 6-P VIA hexokinase
  2. Fructose can enter glycolysis as glyceraldehyde-3-P after conversion to glyceraldehyde via aldose B and conversion of glyceraldehyde to glyceraldehyde-3-P VIA triose kinase.
54
Q

Fructose metabolism is (1) than glycolysis because it bypasses the (2) and there is no (3).

A
  1. Faster
  2. Rate limiting steps
  3. PFK-1 or 2 regulation
55
Q

Galactose can enter glycolysis as glucose-6-P. What are the steps and enzymes used.

A
  1. Galactose to Galactose-1-P via galactokinase.
  2. Galactose-1-P to UDP-galactose
  3. UDP-galactose to UDP-glucose
  4. UDP glucose to Glucose-1-P via GALT
  5. Glucose-1-P to glucose-6-P
56
Q

What is the rate limiting enzyme in Galactose metabolism?

57
Q

What is Galactosemia, and deficiency in what enzyme causes it?

A
  • Disrupted galactose metabolism
  • leads to cataracts, lethargy, and retardation
  • deficiency in galactose-1-phosphate uridyl transferase (GALT)
58
Q

What causes an accumulation of galactose and galactitol in blood and urine?

A
  • deficiency in galactokinase
59
Q

What is the Pentose Phosphate Pathway?

A
  • another oxidative pathway for glucose metabolism
  • produces no energy
  • produces the sugar for DNA and RNA formation
  • Produces NADPH
60
Q

Where does the Pentose Phosphate Pathway Take Place?

61
Q

What is the rate limiting step of the pentose phosphate pathway?

A

G6PD

Glucose-6-phosphate dehydrogenase

62
Q

What are the major steps of the PPP?

A
  1. Conversion of G6P to 6-p-lactone via G6PD.

2. Reduction of NADP+ to NADPH

63
Q

Study PPP from notes

A

It is too complicated to make note cards on lol

Exam 1 (7 decks)

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