Review Cards Flashcards
Name differences in Hexokinase and Glucokinase (location, affinity, regulators)
Rxn: Glucose –> G-6-P
Glucokinase: in liver, low affinity, high Km for glucose
- Glucose –> cytosol
- F-6-P –> nucleus
- Insulin –> increase expression (inducible)
Hexokinase: outside liver, high affinity, low Km for glucose
- G-6-P negative feedback
- Non-inducible, constitutive
What is the main activator of PFK-1?
F-2,6-bisP allosteric activator
Reaction: PFK-1: F-6-P –> F-1,6,-P
Other activators: AMP, ADP
Inhibitors: ATP, Citrate
How is PFK-2 differentially regulated in liver and muscle under fasting?
Liver: PFK-2 kinase domain is phosphorylated by glucagon/Epi –> inhibited –> no F-2,6-bisP –> inhibit hepatic glycolysis
Muscle: PFK-2 phosphatase domain is phosphorylated by Epi, so kinase is active –> increased F-2,6-bisP –> activate PFK-1 –> glycolysis active
What are the regulators of Pyruvate Kinase?
[Reaction: PEP –> Pyruvate]
Activated by insulin (de-phosphorylation) and F-1,6-bisP (feed forward)
Inhibited by glucago/Epi (phosphorylation), ATP, Alanine
What are the 4 fates of Pyruvate?
- Transamination –> Alanine
- Pyruvate Carboxylase –> Oxaloacetate
- LDH –> Lactate
- PDH –> Acetyl CoA
What are the names of the 2 shuttles that regenerate NAD+?
- Malate-Aspartate
- Glycerol-Phosphate
Use them to regenerate NAD+ in the mitochondria because NADH can’t cross the membrane; they can be reoxidized by ETC, so get a lot more ATP from this than making lactate
What is the reaction catalyzed by LDH? What is the point? How is it different in skeletal and heart muscle?
Pyruvate + NADH+ –> Lactate + NAD+
- To regenerate NAD+
- Skeletal m. will convert Pyruvate –> Lactate (2 ATP)
- Heart m. will convert Lactate –> Pyruvate for TCA
What is catalyzed by PDH? How is it regulated?
Pyruvate + CoASH + NAD+ –> Acetyl CoA + NADH
- Needs vitamin cofactors
- Acetyl CoA, NADH are feedback inhibitors
What is Galactosemia?
Deficiency of Galactose-1-P-Uridyltransferase –> accumulation of galactose –> increase of galactitol –> cataracts, jaundice, enlarged liver, kidney damage, brain damage
What are the 3 sources of Acetyl CoA?
- Glycogen –> Glucose –> Pyruvate –> Acetyl CoA
- TAGs –> FFA –> Acetyl CoA
- Proteins –> a.a. –> Acetyl CoA
What are the 3 fates of Acetyl CoA?
- TCA
- Ketone bodies
- Sterols, FAs
How many ATP are made with each cycle of TCA?
9 ATP + 1 GTP = 10 ATP
What does isocitrate dehydrogenase control? How is it regulated?
Fine control of TCA
Reaction: [isocitrate –> a-ketoglutarate]
Activated by: ADP
Inhibited by: ATP, NADH
What does a-ketoglutarate dehydrogenase control? How is it regulated?
Fine control of TCA
Reaction: [a-ketoglutarate –> succinyl coA]
Activated by: ADP, Ca2+
Inhibited by: ATP, GTP, NADH, Succinyl coA
What are the non-carbohydrate precursors used to make glucose in Gng?
Pyruvate, Lactate, Glycerol, Glucogenic a.a.