Hormonal Regulation and Energy Flashcards
Liver Response to Fed State
Increase storage of glucose carbons
Glucose to glucose 6P
Glycogen synthesis
Glycolysis
Liver use of Glucose during High Insulin
No use of glucose
Inhibits glycogenolysis
Inhibits gluconeogenesis
Inhibit G6P to Glucose
Properties of PFK(1)
Conversion of Fructose 6P to Fructose 1,6BP
Activated by AMP, Fructose 2,6BP
Inhibited by ATP and Citrate
nb: fructose 1,6BP feeds forward to Pyruvate Kinase
Properties of PFK2-F26BPase Enzyme
Conversion of F6P to F26BP is promoted by high insulin
Glucagon activates PKA
PKA phosphorylates and deactivates PFK2
Activators of mTORC1
Amino Acids during Fed State (from meal)
Activation of Insulin Receptor to stimulate PKB (Akt)
Role of mTORC1
Inhibits production of Insulin Receptor
Activates SREBP1c
Role SREBP1c
increases Glucokinase and pyruvate kinase (proglycolysis)
Lipogenic enzymes
Increases expression of Glucose 6 Phosphate Dehydrogenase in PPP
Relationship between FOX01 and Insulin
Insulin Deactivates FOX01 via Akt
Role of FOX01
FOX01 promotes gluconeogeneiss and HDL synthesis
Actions of PKA
Activates phosphorylase kinase (activates gluconeogenesis)
Phosphorylates and deactivates PFK2
Activates CREB (transcription factor for gluconeogenesis)
Phosphorylates and deactivates pyruvate kinase
Phosphorylates and activates HSL to break down lipids
What is the first organ to respond to glucagon?
Liver
Where are catecholamines produced and by what major Amino Acid/ Enzyme
Catecholamines are made in the medulla of the adrenal gland
Derived from tyrosine via tyrosine hydroxylase
Main signaling protein for low energy
AMP Kinase
senses low ATP/AMP levels
AMP kinase is activated by
Biguanides
Phenobarbital
Caloric Deprivation
Result of active AMP kinase
Increase Catabolic Reactions / Decrease Anabolic Reactions
Increase glycolsis / Decrease Lipid Synthesis
Increase FFA Oxidation / Decrease Cell Cycle Progression
Increase Autophagy / Decrease Gluconeogenesis