Glycogenolysis/
Glycogen Synthesis
Glycogen Synthesis
Insulin will ______ glycogenolysis and _______ glycogen synthesis
decrease, increase
Where does gluconeogenesis occur?
the liver
Lipolysis must be regulated by ________
Hormones
What is the meaning of allosteric regulation?
Regulators/enzymes activate or repress an active site
Which hormone is responsible for increasing lipolysis?
epinephrine
What are the allosteric vs. hormonal ways to activate Phosphorylase?
Allosteric regulation (non-hormonal): activation of phosphorylase kinase through calcium and AMP
Hormonal mechanism:activate phosphorylase kinase includes epinephrine/cAMP Cascade
An increase in epinephrine will inhibit/activate which enzymes in the liver?
Inhibit: PFK (glycolysis) by turning off the kinase side of the bifunctional enzyme
Activate: Fructose 1,6- bisphosphatase (gluconeogenesis) by turning on the phosphatase side of the bifunctional enzyme
What are the 3 components of Lipolysis that will be sped up by PKA?
1. CGI-58
2. Perilipin I
3. HSL (Hormone Sensitive Lipase)
How is AMPK activated?
Increases in AMP and calcium during exercise
What would be the effect on glycogenolysis if PKB can not be activated?
Glycogenolysis would continue because there would be no insulin available to deactivate Phosphorylase
You are in a postprandial state. Which hormone will be dominant?
The postprandial state means after eating, so the increase in blood glucose will cause insulin to be increased
Do you want gluconeogenesis to be increased or decreased in the liver during exercise? Why?
Increased because you are gaining more free glucose to break down for ATP
How would a faulty beta-adrenergic receptor impact lipolysis?
It would decrease lipolysis because epinephrine would be unable to bind in order to start the cAMP Cascade. PKA would not be available to increase the activation of CGI-58, Perilipin I, and HSL
How is CAT I activated and deactivated?
Activated: increases in AMPK, acyl CoA, and carnitine
Deactivated: increases in Acetyl CoA Carboxylase and malonyl CoA
What are the two ways that PP1 increases glycogen synthesis?
PP1 activates Glycogen Synthase a
PP1 deactivates Phosphorylase in order to stop glucose breakdown
You have a major increase in calcium and AMP that activates Phosphorylase Kinase. How will this impact glycogenolysis?
Glycogenolysis would increase because Phosphorylase Kinase will activate Phosphorylase, so that glycogen can be broken down
Insulin decreases PKA and increases fructose 2,6-bisphosphate. This will _____ glycolysis in the liver
Increase
How is Lipolysis slowed through insulin?
cAMP is turned into AMP through phosphodiesterase 3B
Phosphodiesterase 3B his slows down lipolysis by deactivating CGI-58, Perilipin I, HSL
How is PFK activated and deactivated?
Activated: Increases in AMP and Fructose 2,6-bisphosphate in the liver
Deactivated: Increases in ATP
How does Type II Diabetes affect lipolysis?
Lipolysis is increased because Phosphodiesterase 3B can not be activated to stop lipolysis
What are the ways that Insulin increases glycogen synthesis?
Increase GLUT 4 translocation w PKB
Deactivate GSK3 w PKB
Deactivate phosphorylase w PP1
Activate glycogen synthase w PP1
How will hyperglycemia be reversed through insulin?
Increase in PFK (glycolysis) and decrease in fructose 1,6-bisphosphatase (gluconeogenesis)
GLUT 4 increased, glycogen synthesis increased
Free glucose goes down
How will lipolysis be affected by an increase in AMPK?
Increase: AMPK increases the translocation of FAT-CD36, which will allow more fatty acids to enter the cell in order to go through lipolysis
How is Pyruvate Dehydrogenase activated and deactivated?
Activated: Activation of PDH Phosphatase through calcium and magnesium, deactivation of PDH Kinase through an increase in pyruvate and ADP
Deactivation: Activation of PDH Kinase
What are the 3 reasons why we want AMPK active?
Increase glucose availability because of increased translocation of GLUT4
Increase fatty acid availability because of increased translocation of FAT/CD36
Decrease Acetyl CoA Carboxylase which decreases malonyl-CoA and allows CAT1 to stay active