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Flashcards in Glycogensis Deck (16):

what is the primer of glycogen synthesis? Describe it

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


Glucosylation vs Glycosylatin

Glucosylation is glucose binding to soemting

Glycosylation is any time of carb binding to something 


Phase 1 of glycogen synthesis 

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 




Phase 2 of Glycogen Synthesis

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



Phase 3- branching


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


What 2 enzymes are regulated in glycogen synthesis?

The glcogen phosphrylase (glucokinase/hexokinase)-

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


What hormones upregulate and down regulate synthesis of glycogen

Upregulated- insulin

Dpwn- glucagon and Epinephrine


What regulates the glycogen phosphorylase in the glycogen degradation

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


Hormonal steps of glycogen degradation 

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 




regulation of glycogen synthesis 

Upregulated glycogen synthesis when Glucose 6-p


only main allosteric of glycogen sythase


hormonal regulation of glycogen synthess 

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. 


major function of glucagon and what does it work on

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 


What does epinephrine do in liver and muscle

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


Ca2+ effect on muscle

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 


Why are children and premature kids more likely to be hypoglcemic

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