EXAM3_L34_Hexose_Monophosphate_Shunt_PPP Flashcards

1
Q

What are the required enzymes for oxidative HMP

A

G6PD (rate limiting)

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2
Q

What enzyme and coenzyme required for HMP non-oxidative forward and reverse reactions?

A

Transketolase (req. TPP)

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3
Q

Forward non-oxidative branch: reactants and products

A

Ribose5P –> Fructose 6P and Glyceraldehyde3P

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4
Q

Reverse non-oxidative branch reactants and products?

A

Fructose 6p and glyceraldehyde3p&raquo_space; ribose 5p

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5
Q

How is oxidative HMP regulated?

+ means “activated by”
- means “inhibited by”

A

+ G6P
+NADP+

  • NADPH
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6
Q

How is non-oxidative HMP regulated?

A

Its not! — some influence by TPP (co-enzyme required by Transketolase)

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7
Q

What is the purpose of Oxidative HMP?

Makes 4 things:

A

NSFG

  1. FA synthesis (liver, adipose, lactating gland)
  2. Steroid Synth (testes, ovaries, placenta, adrenal ctx)
  3. Glutathione reduction in RBC’s (antioxidant)
  4. Ribose5P required for nucleotide synthesis
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8
Q

What is the purpose of non-oxidative HMP?

A

When body doesn’t need Ribose5P they can be converted and fully oxidized for energy

  • Allows Metabolism of dietary 5-carbon sugars
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9
Q

What effect does Citrate in the cytosol have on HMP shunt?

A

Citrate inhibits PFK1 (glycolysis stops)
G6P builds up and enters HMP> increases NADPH >

  • FA synthesis or Glutathione reduction or other anabolic processes

Citrate X PFK1 = G6P>HMP>NADPH>FA

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10
Q

What are the two sources of NADPH?

A

Malic enzyme + Oxidative HMP

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11
Q

The RBC, Cornea, and Lens are tissues without mitochondria. Where do they get NADPH from?

A

Oxidative HMP only!

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12
Q

Glutathione

A

Tripeptide with SH group that donates electrons to H2O2

oxidized glutathione is reduced again by NADPH

glutathione synthesis requires ATP

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13
Q

What are the 3 major dietary sources of Fructose?

A
  1. Sucrose (glucose + fructose)
  2. Free fructose (fruits and honey
  3. High fructose corn syrup (many prepared foods)
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14
Q

Fructose can enter the cells regardless of insulin levels what else makes it unique from glucose?

A

Extremely poor illicitor of insulin secretion

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15
Q

Why if high fructose SO FATTY!

A

Fructose enters glycolysis downstream of the PFK1 regulation. (as glyceraldehyde 3 phosphate)

Fructose&raquo_space; DHAP + Glyceraldehyde

  1. Fructose Metabolism is FASTER
  2. DHAP can be converted to Glycerol3P (TAG synth)
  3. Rapid metabolism increases Acetyl-CoA in cytosol (activating FA synth)
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16
Q

Aldose Reductase has a high Km for galactose and is not usually a problem but if galactose is high then..What is the role aldose reductase in galactose metabolism?

A

aldose reductase converts galactose to GALATITOL

  • Galactitol causes cataracts seen in galactose disorders
17
Q

3 steps of galactose metabolism

A
  1. Galactokinase (sugar trap)
  2. G1PUT
  3. C4Epimerase
    - UDP glucose used for:
    - glycolysis, gluconeogenesis, lactose in mammary glands, glycoproteins, glycolipids, GAGS
18
Q

If a person is galactose deficient how does the body compensate?

A

Body can still make UDP galactose from UDP-glucose via C4epimerase

19
Q

What can be made with galactose metabolism

(UDP-glucose and UDP-Galactose)?

A

UDP glucose- enter glycolysis, gluconeogenesis

UDP galactose - makes

  1. Lactose,
  2. Glycoproteins
  3. Glycolipids
  4. GAGs
20
Q

Galactokinase deficiency
What is built up?
What is the build up converted to? what converts it?

A

Build up of Galactose in blood, urine, and cell

  • Aldose reductase converts galactose to Galactitol
  • draws fluid into lens, nerves, kidneys– Damage and cell protein precipitation

CATARACTS

21
Q

What is the pathology of galactokinase deficiency?

A

CATARACTS

Galactitol -draws fluid into lens, nerves, kidneys– Damage and cell protein precipitation

22
Q

Aldolase B deficiency

A

Fructose poisoning
Fructose-1P trapped in cells & Accumulates
-HYPOGLYCEMIA-liver failure- death

CUT FRUCTOSE and SUCROSE from DIET

23
Q

Fructokinase deficiency

A

Benign. fructose in urine