Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
17 Cards in this Set
- Front
- Back
|
What is glycogenolysis?
|
Breakdown of glycogen to maintain blood glucose
|
|
|
What is gluconeogenesis?
|
Synthesis f glucose from non-carb precursors (lactate, pyruvate, citric acid interm and the C-skeletons of most aa)
|
|
|
Why can't FA be used as glucose precursors?
|
Can't convert acetyl CoA to OAA in mammals, .: can't use FA in gluconeogenesis
|
|
|
What is the starting material for gluconeogenesis?
|
OAA (.: all precursors must first be converted to OAA)
|
|
|
In what ways is gluconeogenesis the reverse of glycolysis?
|
Glycolysis: Start with glucose
Gluconeo: Produce glucose Glycolysis: Produce ATP Gluconeo: Use ATP Glycolysis: Produce NADH Gluconeo: Use NADH |
|
|
In what way is gluconeogenesis not the reverse of glycolysis?
|
Use dif enz (esp for irrev steps)
-HK=> Glucose-6-phosphatase -PFK=> FBPase -Pyruvate kinase=> Pyruvate carboxylase and PEPCK |
|
|
How do you get PEP from Pyruvate?
|
1) Pyruvate --> OAA
enz: Pyruvate carboxylase Carboxylation 2) OAA --> PEP enz: phosphoenolpyruvate carboxykinase (PEPCK) -Decarboxylation (provides the free E req'd to do gluconeogenesis) -Hydrolyze GTP and add the P to get PEP |
|
|
What enz regulates Pyruvate carboxylase?
|
Acetyl CoA
-if CAC interm are being metabolized through cataplerotic rxns, have less OAA so CAC slows down -.: less Acetyl CoA can be used by CAC, .: its [ ] inc and activates biotin gp of Pyruvate Carboxylase -Pyruvate carboxylase has anaplerotic role of inc [OAA] **If CAC being inhibited by high NADH or ATP, the OAA is used for gluconeogenesis |
|
|
Why is metabolic transport required between the mito and cytosol for gluconeogenesis to take place?
|
-OAA is in the mito, enz for PEP--> glucose are in the cytosol
-PEPCK can be in either the mito or the cytosol. If its in the mito, can convert OAA to PEP in the mito and then PEP can be transported into the cytosol -If PEPCK in the cytosol, OAA must get to the cytosol before it can be converted to PEP. To do this, must convert OAA to malate or aspartate and then use the malate-aspartate shuttle to take it from mito to cytosol |
|
|
What are the 2 routes to get OAA into the cytosol? (malate (route 2) or aspartate (route 1))
|
Route 2
-NADH is transported with OAA -NADH reduces OAA to malate, which is transported to cytosol and then oxidizedback to OAA and NADH (so route 2 req'd under most conditions for gluconeogenesis) Route 1 -LACTATE is the precursor lactate--> pyruvate produces NADH (opposite of lactate DH rxn used in anaerobic conditions after glycolysis) -So OAA gets converted to Aspartate and shuttle to the the cytosol, when its converted back to OAA (but don't need to use NADH) |
|
|
Why is differential regulation required for gluconeo and glycolysis?
|
-Have dif enzymes to differntially regulate the 2 processes (don't want both happening at the same time)
-Regulation at 3 key ptns: Step 1,Step 3 and step 10 of glycolysis (HK, PFK and PK) |
|
|
Net cost of glycolysis + gluconeogenesis?
|
2ATP + 2GTP + 4H2O --> 2ADP + 2GDP + 4 Pi
=> cost E to go glucose=> pyruvate => glucose |
|
|
How is gluconeogenesis regulated in the liver?
|
Allosteric inhibition and covalent modification
-F2,6P: inhibits FBPase, activates PFK -Alanine: inhibits PK and P inactivates PK (dif isoform of PK in muscles, since you want glycolysis running, no gluconeo in muscles) -Acetyl CoA: activates Pyruvate CArboxylase -PEPCK: regulated at the transcriptional level, which is controlled by hormones |
|
|
Where does gluconeogenesis take place?
|
Kidney and liver
|
|
|
What happens when blood glucose lvls are low?
|
Activate gluconeogenesis
-Glucagon inc -acivates adenylyl cyclase, inc [cAMP], which activates PKA, which P PFK-2 (inhibits) and P FBPase2 (activates), leading to a dec in F2,6P -Low F2,6P means PFK is not activated .: FBPase is not inhibited and gluconeogenesis continues |
|
|
What is the Cori cycle?
|
How muscle and liver participate in a metabolic cycle through the bloodstream.
-During exercise, E is used up by muscles 0in intense exercise, rapid glycolysis, mito can't keep up so convert excess pyruvate--> lactate -lactate leaves muscle and goes to liver, where it is reconverted to glucose through gluconeogenesis **This cycle occurs between 2 tissues, not just 1 cell/tissue** |
|
|
Describe alcohol metabolism.
|
-Produces a lot of NADH
-in liver, high NADH/NAD+ ratio means NADH from the alcohol is the main source of ATP -CAC will slow down (inhibited by high NADH) -regenerate NAD+by pyruvate-> lactate and OAA-> malate this reduces substrates for gluconeo, which will slow down -bld glucose lvls drop -alcohol and FA build up in the liver body tricked into thinking E lvls are low so it releases FA that cant be used! |
