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Flashcards in Glycogensis Deck (16)
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1
Q

what is the primer of glycogen synthesis? Describe it

A

It’s glycogenin- which is a self glucosaylating enzyme that can bind one molecule of glucose to Tyrsine

2
Q

Glucosylation vs Glycosylatin

A

Glucosylation is glucose binding to soemting

Glycosylation is any time of carb binding to something

3
Q

Phase 1 of glycogen synthesis

A

Step 1- Glucose + ATP — Glucokinase/hexokinase—> Glucose 6-P + ADP

Step 2- Glucose 6-phosphate– phosphoglucomutase—> Glucose 1-Phosphate

Step 3 Glucose 1-P + UDP— glucose 1-phosphate uridyltransferase–> UDP-glucose + PPi

UDP gluocse is now ready to make glycogen

Sugars often use nucelotides to be activated

4
Q

Phase 2 of Glycogen Synthesis

A

Grow the chain

UDP Synthase+ (Glucose)n—glycogen synthase–> (glucose)N+1 + UDP

The glucose unit joins the growing chain without the phosphates– intitally we start with the amylose chain then we branch

5
Q

Phase 3- branching

A

We now have a growing amylose chain (at least 11 residues) and we take 7units from the amylose chain with a branching enzyme and place them on the amylose chain making a branching point

Remember at the center of glycogen it’s very branched. Every 4 glycogen there is a branch point

6
Q

What 2 enzymes are regulated in glycogen synthesis?

A

The glcogen phosphrylase (glucokinase/hexokinase)-

the glycogen sythase-adds active UDP- glucose to growing bond

7
Q

What hormones upregulate and down regulate synthesis of glycogen

A

Upregulated- insulin

Dpwn- glucagon and Epinephrine

8
Q

What regulates the glycogen phosphorylase in the glycogen degradation

A

Glycogen— glycogen phosphorylase–> Glycogen 1-P (+remaining chaing of glycogen)

Down regulated by G-6-P, glcuose (liver) , and by ATP

***ATP regulation is less effected in the liver because glycogen degradation is for glucose blood regulation***

Upregulated by Ca2+ (muscle b/c it’s realeased during muscle work) and AMP

9
Q

Hormonal steps of glycogen degradation

A

Insulin- Dephos

Glucagon and Epinephrine- Phos

  1. Hormones hit the cells Glucagon receptors and epi hits the beta adrengic receptor
  2. This G-protein activaion produces cycylic AMP which activates protein Kinase A
  3. Kinase A phosphorylates a regulatory enzyme glycogen phosphprylase kinase( in phosphrylated form this enzyme is ACTIVE)
  4. When Glycogen phosphorylase kinase is active is activates glycogen phosphorylase causing glycogen degradation

insulin would have phosphoprotein phosphatase would dephos and inactive phosphorylase kinase and no degradation

10
Q

regulation of glycogen synthesis

A

Upregulated glycogen synthesis when Glucose 6-p

only main allosteric of glycogen sythase

11
Q

hormonal regulation of glycogen synthess

A

insulin depos

Glucagon/Epi phosphoylate

**Glycogen synthase when phosphorylated is inactive.***

So when glucagon and epi bind to G protein and increase in cAMP, increae in Kinase A and phos of glucagon synthase we have an inhibition on glycogen synthesis. Makes sense when we have alot of glucagon we aren’t making glycogen for storage but using it for immediate use.

12
Q

major function of glucagon and what does it work on

A

It stimulates degradation and inhibits glycolysis at the level of 6-phosphofructose-1-kinase (PKF-1) and pyruvate kinase so allows for quikc increase in blood glucose

Major function- mobolize glycogen when food intake is low

13
Q

What does epinephrine do in liver and muscle

A

If it goes though Beta it works that same as Glucagon to inhibit glycolysis at the level of pyruvate kinase and PFK-1

If it’s at an alpha membrane it activates Phospholipase C releasing Ca2+ from the ER–> activate phosphorylase kinase– activates glycogen phosphorylase tsimulating breakdown of glycogen

Muscle use glucose for there own need so here epinephrine doesn’t inhibit glycolysis

In the heart Epi stimulates glycolysis by PFK-2?? review this part

14
Q

Ca2+ effect on muscle

A

Stimulates the degradation of muscle from a neve impulse there is membrane depol releasing Ca2_ from SR which activates phosphorylase kinase which activates glycogen phosphorylase and inactivates glycogen synthase

15
Q

Why are children and premature kids more likely to be hypoglcemic

A
  1. Larger brain/body ratio so they need more glucose to CNS
  2. Newborns have limited ketogenosis which would be the alternative to glucose for CNS
  3. Gluconeogenosis from lactate and alanine is limited form newborns more severe in premature and skinny babies
16
Q
A