Gluconeogenesis Flashcards
glucose-6-phosphatase is only present in which organs?
ones that carry out gluconeogenesis:
liver and kidney
bc it allows glucose to leave the cell
what state is gluconeogenesis performed in?
fasting / starvation state
what is the energy investment amount for gluconeogenesis?
total / per glucose
- 4 ATP
- 2 GTP
- 2 NADH
what is reciprocal regulation?
two competing pathways try to occur at the same time, but the same signal has opposite effects on them (turns one off while turning the other on)
if both are on, substrate of one is the product of other -> endless circle
in fasting/starvation state, +glucagon signaling does what to glycolysis and gluconeogenesis?
glycolysis OFF
gluconeogenesis ON
in fed state, +insulin signaling does what to glycolysis and gluconeogenesis?
glycolysis ON
gluconeogenesis OFF
when energy charge is LOW, what pathway is on?
glycolysis, to acquire energy from glucose degradation
when energy charge is HIGH, what pathway is on?
gluconeogenesis, to use our abundant energy to make glucose
how does energy charge being low activate glycolysis?
AMP stimulates PFK-1
how does energy charge being low deactivate gluconeogenesis?
AMP deactivates fructose-1,6-BPase
ADP deactivates PEP carboxykinase, and pyruvate carboxylase
how does energy charge being high deactivate glycolysis?
ATP deactivates PFK-1, and pyruvate kinase
how does energy charge being high activate gluconeogenesis?
absence of its inhibitors, AMP and ADP allows gluconeogenesis to stay on
in a diabetic individual, what happens in regard to gluconeogenesis after eating a meal?
insulin is not released OR insulin signal receptors on cells do not work
PEP carboxykinase is not inhibited by insulin, so gluconeogenesis stays ON
cells (including liver) stay in fasting/starvation state -> glucose continues to be produced while we’re already hyperglycemic
what happens when Acetyl-CoA inhibits PDH from making more Acetyl-CoA?
what state is this in?
diverts pyruvate to gluconeogenesis
fasting/starvation state
how does alcohol inhibit gluconeogenesis?
depletes cytoplasmic NAD+ pool
malate cannot be converted back to OAA in cytoplasm
