Glycogensis

Question 1

what is the primer of glycogen synthesis? Describe it

Answer 1

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

Question 2

Glucosylation vs Glycosylatin

Answer 2

Glucosylation is glucose binding to soemting

Glycosylation is any time of carb binding to something

Question 3

Phase 1 of glycogen synthesis

Answer 3

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

Question 4

Phase 2 of Glycogen Synthesis

Answer 4

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

Question 5

Phase 3- branching

Answer 5

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

Question 6

What 2 enzymes are regulated in glycogen synthesis?

Answer 6

The glcogen phosphrylase (glucokinase/hexokinase)-

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

Question 7

What hormones upregulate and down regulate synthesis of glycogen

Answer 7

Upregulated- insulin

Dpwn- glucagon and Epinephrine

Question 8

What regulates the glycogen phosphorylase in the glycogen degradation

Answer 8

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

Question 9

Hormonal steps of glycogen degradation

Answer 9

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

Question 10

regulation of glycogen synthesis

Answer 10

Upregulated glycogen synthesis when Glucose 6-p

only main allosteric of glycogen sythase

Question 11

hormonal regulation of glycogen synthess

Answer 11

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.

Question 12

major function of glucagon and what does it work on

Answer 12

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

Question 13

What does epinephrine do in liver and muscle

Answer 13

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

Question 14

Ca2+ effect on muscle

Answer 14

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

Question 15

Why are children and premature kids more likely to be hypoglcemic

Answer 15

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