carbohydrate metabolism cont Flashcards

1
Q

what is the pentose phosphate pathway

A

*source of nucleotides within cell, has 2 phases

-somewhat anabolic pathway, making mol larger

Oxidative

  • oxidation of glucose 6-P → produces 2 NADPH and ribulose 5- phosphate (=> ribose-5-phosphate)
  • NAD used as oxidizer

Non-oxidative: isomerization/rearrangements

  • glycolytic intermediates
  • glucose 6-phosphate
  • xylulose 5-phosphate (modulator of phosphatase that stimulates liver PFK-2)
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2
Q

what are the produces of the oxidative phase

A

→ for the synthesis of nucleotides (ribose 5-phosphate)
→ reductive biosynthesis (NADPH), for e.g. fatty acids

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3
Q

what are the products of the non oxidative phase

A

→ replenish glucose 6-phosphate and glycolytic intermediates
→ source of xylulose 5-phosphate.

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4
Q

explain non oxidative phase

A
  • start with rubose 5 phos to go to glucose 6 phos
  • why? part of this pathway is generating fatty acids adn the other is generating nucleotides
  • if need for DNA RNA is low, take the ribulose 5 phosphate and reshuffles it to go back to glucose 6 phosphate (dont want it to build up)

*dont memroize intermediates and all enzymes,

  • esentially going from 5 carbon molecule to 6 carbon molecule
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5
Q

what do the diff intermediates and enzymes do in non oxidative phae

A

Transaldolase/transketolase can transfer 2/3 carbon atoms between sugar phosphates

This allows you to rearrange 5C molecules into 6C molecules

The final 3C sugars are glyceraldehyde-3P, which can turned into glucose-6P by gluconeogensis steps

Net: 6 x 5C –> 5 x 6C

*no ent gain or los of energy, point is to recycle the ribuclose 5 phosphate

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6
Q
A
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7
Q

how do you regualte the pentose phosphate pathway

A

Glucose 6-phosphate dehydrogenase is:

  • stimulated by NADP+
  • inhibited by NADPH

*regulated by redox state of the cytosol

  • glucose 6 phos is largly commited to glycolysis to generate ATP
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8
Q

what is glycogen

A

polymer of glucose (storage)

  • quick source of energy
  • in the liver we have glycolysis and control of blood [glucose]
    mucle: glycolysis
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9
Q

explain glycogen synthesis

A

Glycogen Synthesis – making the precursor:

  1. glucose 6-P –> glucose 1-P: Phosphoglucomutase
  2. glucose 1-P + UTP —> UDP-glucose + PPi: UDP-glucose pyrophosphorylase

UDP-glucose then acts as an activated sugar donor

*by making glycogen we are polymerizing glucose mol and utilizing UDP to do that, glycogen synthase is the enzyme sticking sugar on the growing chain, spitting out UDP

*net result is get a new non reducing end, elongated chain

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10
Q

what is glycogenolysis

A
  • glycogen breakdown

*glycogen phosphorylase reaction

**RECALL: glycogen synthase is inhibited by phosphorylation (PKA and GSK3)

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11
Q

how is glycogen metabolism regulated

A
  • Recall: Glycogen synthase is inhibited by phosphorylation, and glycogen phosphorylase is activated by phosphorylation
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12
Q

what is the role of Glycogen phosphorylase b kinase

A

Role in glycogen metabolism

  • phosphorylates glycogen phosphorylase
  • activates glycogen phosphorylase

***The activity of glycogen phosphorylase b kinase is stimulated by PKA-mediated phosphorylation

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13
Q

What is the role of glycogen phosphorylase a phosphatase

A
  • dephosphorylates glycogen phosphorylase
  • inhibits glycogen phosphorylase
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14
Q

Glycogen phosphorylase is activated by

A

phosphorlyation

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15
Q

wht is role of phosphorylase B kinase

A

phosphorylates glycogen phosphorylase

activates glycogen phosphorylase

The activity of glycogen phosphorylase b kinase is stimulated by PKA-mediated phosphorylation

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16
Q

what is the role of Glycogen phosphorylase a phosphatase

A
  • dephosphorylates glycogen phosphorylase
  • inhibits glycogen phosphorylase
17
Q

what is the role of glycogen phosphorylase

A
  • glucose sensor
  • Glucose binding of phosphorylase a has an allosteric effect
  • This favours dephosphorylation (and inactivation) by phosphorylase a phosphatase
  • allosteric sites are empty when glucose is low, phosphorylated amino acids are tucked away so cant be dephosphorylated
  • when glucose levels are high, binding to allosteric sites, conformational change, phosphate groups are exposed and available to be chewed off

*insulin inc activity of phosphatase (makes it less active)

  • glucose favours dephosphorylation by making sites availabile to phosphorylase a
18
Q

how do glycogen synthase and phosphorylase relate

A
  • reciprocally regulated by phosphorylation
  • phosphorylation of gly syn a inactivates glycogen synthase b
  • glycogen phosphorylase b is phosphorylated becoming active glycogen phosphorylase a

*protein phosphatase dephosphorylases both glycogen synthase b and glycogen phosphorylase a

19
Q

exaplin PKA mediated regulation of carbohydrate metabolism in the liver

A
  • PKA regulation ensures that low blood sugar leads to increased glycogen breakdown, and decreased glycogen synthesis and glycolysis
  • low blood glucose stimulates glucagon synthesis which inc concentration of cAMP which inc PKA
  • PKA inc levels of phosphorylase kinase, inc glycogen phosphorylase which inc glycogen breakdown
  • PKA dec glycogen synthase, dec glycogen synthesis
  • PKA INC FBPase-2, DEC PFK-2, this dec [F26BP], which dec PFK-1 which dec glycolysis
  • PKA dec pyruvate kinase L which dec glycolysis
20
Q

how do hormones regulate enzyme activity

A
  • coordinate tissue specific metabolism
  • epinephrine has differential effects depending on the tissue
  • ep in muscle inc glycogenolysis (break down glycogen)
  • ep dec glycolysis in liver and inc glycolysis in the muscle
  • ep inc gluconeogenesis in the liver
21
Q

explain tissue specific metabolism

A
  • Myocytes lack glucagon receptors
  • Muscle pyruvate kinase is not phosphorylated by PKA

• Muscle lacks gluconeogenic enzymes
• Muscle lacks a key enzyme for glucose export
→ Muscle uses stored glycogen and glucose for itself