Random Mignery

Question 1

Hexokinase

Answer 1

Present in all cell types
Converts glucose to G6P
Allosterically inhibited by G6P
Constitutive enzyme and non-inducible, constant amount
Saturated at low glucose concentrations

Question 2

Glucokinase

Answer 2

Present in liver and pancreas
Converts glucose to G6P
Translocation between the nucleus (inactive) and cytosol (active)
F6P will decrease activity by promoting translocation to nucleus
Glucose and F1P increases GK activity by promoting translocation to cytosol
Inducible enzyme, enzyme synthesis will increase with insulin
Not saturated at physiological glucose conditions

Question 3

Allosteric regulation of PFK-1

Answer 3

PFK-1 converts F6P to F1,6P
Positively regulate: High concentrations of F2,6BP, AMP, and ADP
Negatively regulate: High concentrations of ATP and citrate

Question 4

F2,6BP activity in terms of glucose levels

Answer 4

High blood glucose and high insulin, increased F2,6BP

Low blood glucose, high glucagon and epinephrine is low F2,6BP

Question 5

Hepatic PFK-2 is phosphorylated in what domain and in response to what, and what effect will this have

Answer 5

Phosphorylated in the kinase domain by PKA in response to glucagon or epinephrine. This will inhibit PFK-2 and thus inhibit glycolysis

Question 6

What is the signaling pathway for glucagon inhibiting PFK-2 (hepatic)

Answer 6

Glucagon binds to glucagon receptor, activates G subunit, activates adenylyl cyclase, which makes cAMP, which will activate PKA, which will phosphorylate PFK-2, inhibiting production of fructose 2,6-BP

Question 7

Cardiac PFK-2 is phosphorylated in what domain and in response to what, and what effect will this have

Answer 7

Heart PFK-2 is phosphorylated in the phosphatase domain, which inhibits the phosphatase activity, leading to increased PFK-2 activity. This is in response to epinephrine, but not glucagon

Question 8

Signaling pathway in heart and muscle for ephinephrines effect on PFK-2

Answer 8

Epi binds to beta adrenergic receptor, activates adenylyl cyclase, which makes cAMP, which activates PKA. PKA will phosphorylate cardiac and muscle PFK-2 kinase, activating it, which then makes F2,6BP, which is then able to go positively regulate PFK-1

Question 9

Pyruvate kinase does what, and how is it regulated

Answer 9

Pyruvate kinase will turn phosphoenolpyruvate into pyruvate
When pyruvate kinase is phosphorylated, it is less active, and when its dephosphorylated, its more active
High blood glucose levels and insulin will lead to more dephosphorylated and more active pyruvate kinase via phosphoprotein phosphatase, and vice versa

Question 10

Positive and negative regulators of pyruvate kinase

Answer 10

Fructose 1,6 BP is a positive regulator

ATP and alanine are negative regulators

Question 11

Effect of glucagon and epinephrine on hepatic pyruvate kinase

Answer 11

Phosphorylated and inhibited

Question 12

The glyceraldehyde-3-P dehydrogenase reaction requires a steady supply of what

Answer 12

NAD+

Question 13

NAD+ can be regenerated by what 3 methods, and where are those pathways located

Answer 13

Lactate dehydrogenase, in the cytosol
Malate-aspartate shuttle, in the cytosol and mitochondria
Glycerol-phosphate shuttle in the cytosol and mitochondria

Question 14

Pyruvate goes to lactate with what enzyme

Answer 14

Lactate dehydrogenase

Question 15

Specifically in skeletal muscle, what form of lactate dehydrogenase is there and what does this allow the skeletal muscle to do

Answer 15

LDH5 M4 isozyme, will allow for high bursts of energy

Question 16

In heart muscle, what lactate dehydrogenase isozyme is there and what does it allow for

Answer 16

H4 isozyme and allows for sustained production of energy

Question 17

What happens if you have lactate dehydrogenase A deficiency

Answer 17

Cannot maintain moderate levels of exercise due to an inability to utilize glycolysis to produce ATP needed for muscle contraction. The level of NAD+ becomes limiting during exercise and flux through the glyceraldehyde-3-P dehydrogenase reaction is inhibited

Question 18

Vitamin cofactors for PDH

Answer 18

Thiamine (TPP, B1)
Riboflavin (FAD, B2)
Niacin (NAD, B3)

Question 19

Regulation of PDH, allosterically

Answer 19

NOT regulated by glucagon and epinephrine, the end products inhibit PDH by allosteric inhibition. End products cause the phosphorylation and inhibition of PDH
Phosphorylated pyruvate dehydrogenase is inactive, dephosphorylated is active

Question 20

Regulation of PDH, actual chemicals

Answer 20

NADH and AcCoA will promote inactivation of PDH (allosteric inhibition)
CoASH, NAD+, ADP, and pyruvate will inhibit deactivation of PDH
Mg2+ and Ca2+ will promote activation of PDH

Question 21

What is the metabolic pathway for galactose

Answer 21

Lactose breaks into glucose and galactose
Galactose turns to galactose 1-P via galactokinase
Galactose 1-P turns to glucose 1-P via Gal-1-P uridyltransferase
Glucose 1-P goes to G6P

Question 22

Galactitol is formed under what conditions

Answer 22

In galactosemia, and from galactose. If there is a deficiency of galactokinase and galactose 1-P uridyltransferase

Question 23

Metabolic pathway of fructose

Answer 23

Fructose is transported by GLUT5, and goes to fructose-1-phosphate via fructokinase.
Fructose-1-phosphate goes to glyceraldehyde and DHAP via aldolase B in the liver and erythrocytes (Aldolase A in muscle and aldolase C in brain)

Question 24

What happens to ATP levels when there is a deficiency of aldolase B

Answer 24

Cannot cleave F1P, so all the phosphate is tied up in F1P, so ATP levels drop rapidly