Valencik: Carbohydrate metabolism III Flashcards

1
Q

What two sugars make up lactose?

A

galactose and glucose

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2
Q

What two sugars make up sucrose?

A

fructose and glucose

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3
Q

What sugars make up trehalose?

A

glucose and glucose

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4
Q

How does fructose enter glycolysis?

A

Converted to DHAP or G3P

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5
Q

How does galactose enter glycolysis?

A

Converted to G6P

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6
Q

How does mannose enter glycolysis?

A

Converted to F6P

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7
Q

Most common form of fructose is (blank). Fructose tastes sweeter than (blank). It is less rapidly absorbed in the intestine, but more rapidly (blank).

A

sucrose; glucose; metabolized

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8
Q

What two steps convert Fructose to glycolytic intermediates in the liver?

A

Fructose —> Fructose-1-phosphate via Fructokinase

F1p —> Glyceraldehyde + DHAP
Aldolase B

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9
Q

Which of the following is the slow step in fructose metabolism in the liver?

Fructose —> Fructose-1-phosphate via Fructokinase

F1p —> Glyceraldehyde + DHAP
Aldolase B

A

The first step, so F1P accumulates

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10
Q

Where does F1P enter glycolysis in the LIVER?

A

Bypasses two regulated steps (glucokinase and PFK1) and is converted to DHAP

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11
Q

What steps in glycolysis does F1P stimulate?

What steps does it inhibit?

A

Stimulates glucokinase and pyruvate kinase

Inhibits phosphohexose isomerase and aldolase

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12
Q

Fructose is metabolized faster than glucose, so (blank) directs dietary glucose into glycogen synthesis.

A

fructose-1-phosphate

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13
Q

A mutation in fructokinase leads to this condition

A

essential fructosuria

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14
Q

A mutation in aldolase B leads to this condition and these symptoms

A

fructose intolerance, neusea, vomiting, hypoglycemia, liver damage

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15
Q

Where does fructose enter glycolysis in the MUSCLE?

A

Fructose is converted directly to F6P, so it does not bypass the regulated step of glycolysis (PFK1)

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16
Q

What converts fructose to F6P in muscle? What is required for this reaction?

A

hexokinase; ATP

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17
Q

What is one reason why fructose can be bad for you?

A

Fructose will be converted to F1P in great concentrations, which requires a lot of Pi, which impairs oxidative phosphorylation

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18
Q

3 steps of galactose metabolism

A

Galactose –> Galactose-1-phosphate via galactokinase

Gal1P –> UDP galactose via galactose-1-phosphate uridyl transferase

UDP galactose –> UDP glucose via UDP galactose 4-epimerase

19
Q

If there is a mutation in the enzyme that takes Galactose 1 phosphate to UDP galactose, what condition does this cause?

A

Classic galactosemia, TYPE 1 GALT

Will cause liver damage, vomiting after eating, must avoid milk.

20
Q

If there is a mutation in the enzyme that takes UDP galactose to UDP glucose, what condition does this cause?

A

GALE deficiency TYPE 3

Can be mild or severe

21
Q

Why is early diagnosis essential when there are defects in the metabolism of galactose

A

Galactose-1-phosphate can accumulate and cause vomiting, liver damage, mental deficiency, and cataracts.

22
Q

Why can defects in the galactose pathway lead to cataracts?

A

Deficiency in the Polvol pathway

23
Q

Why is fructose metabolized faster in the liver than in the muscle?

A

In the liver, it enters after the committed step of glycolysis

24
Q

What do nucleated cells use the pentose phosphate pathway for?

A

To generate NADPH

To generate precurosors of nucelotide biosynthesis

25
Q

NADPH is used for reductive biosynthesis of (blank) and cholesterol and for defense against (blank).

A

fatty acids

oxidative

26
Q

Two products of the pentose phosphate pathway

A

Ribose-5-phosphate

NADPH

27
Q

NADPH and R5P can be used in the biosynthesis of these four things

A

fatty acids
cholesterol
neurotransmitter
nucleotides

28
Q

Two branches of the pentose phosphate pathway

A

oxidative

non-oxidative

29
Q

What is the committed step of the pentose phosphate pathway? What is this step dependent on?

A

Glucose-6-phosphate —> 6 phosphogluconate via G6P dehydrogenase

NADP+

30
Q

Availability of (blank) regulates G6PDH

A

NADP+

31
Q

If NADPH is forming faster than it is being used, what happens?

A

NADP+ is decreased and the committed step of the PPP does not proceed

32
Q

What are the most important enzymes in the non-oxidative phase of the pentose phosphate pathway?

A

transketolase and transaldolase

33
Q

What are the products of the non-oxidative phase of the PPP? What is the purpose of the non-oxidative phase?

A

2 F6P and G3P; to generate pentoses that can feed into glycolysis

34
Q

1st rxn of non-oxidative phase: The transketolase reaction coverts two pentose phosphates to a (blank) and a (blank)-sugar phosphate. How many carbons are transferred? What is this reaction dependent on?

A

triose; seven; two carbons; TPP

35
Q

2nd rxn of non-oxidative phase: How many carbons does transaldolase transfer? What is it dependent on?

A

3 carbons; energy and vitamins

36
Q

3rd rxn of non-oxidative phase: How many carbons does transketolase transfer? What are the products of this reaction? What is this reaction dependent on?

A

two carbons; G-3-P and F6P; TPP

37
Q

You can use the pentose phosphate pathway in four different ways.

A
To generate:
NADPH and R5P
NADPH only
Ribose only
NADPH and C2 units for Fatty acids
38
Q

Uses nucleotide-activated sugars derived from glucose in the biosynthesis of glycolipids, glycoproteins and proteoglycans

A

uronic acid pathway

39
Q

The products of the uronic acid pathway can feed into this pathway

A

PPP

40
Q

Why run the PPP in RBCs?

A

To provide the reducing power necessary to protect RBCs from oxidative damage

41
Q

In RBCs, NADPH is used to keep (blank) reduced.

A

Glutathione

42
Q

What protects RBCs from highly reactive oxygen derivatives?

A

Glutathione

43
Q

Why are RBCs affected most by G6PDH deficiency?

A

RBCs cannot synthesize new G6PDH proteins to replace defective ones. Therefore they must protect their proteins from oxidative damage by maintaining a reducing environment in the cell

44
Q

What is one advantage of G6PDH deficiency?

A

malaria resistance