Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

22 Cards in this Set

  • Front
  • Back
Describe the regulation of cholesterol synthesis. What is the name of the enzyme responsible?
very important to regulate cholesterol synthesis b/c cholesterol cannot be degraded in human. HMG-CoA Reductase is the enzyme responsible. Also regulated by Insulin and Glucagon
Discuss the formation of HMG-CoA Reductase.
Formed in the cytosol by Acetyl-CoA, which is normally found only in mitochondria. It is transported to cytosol when cholesterol synthesis is needed.
Why is substrate availability a regulator for enzyme activity? What is velocity?
The more substrate that is available, the faster a reaction will proceed (up to a max velocity). Velocity is product formation / time, or the rate of the rxn/enzyme.
Discuss Product Inhibition, particularly for Hexokinase.
enzyme is inhibited by the DIRECT product that it acts upon to make.

Example - Hexokinase phosphorylates glucose to make G-6-P, which then inhibits Hexokinase when its levels are high enough in the cell.
Why do Allosteric Enzymes show a sigmoidal curve related to velocity and substrate concentration?
Allosteric enzymes have several subunits and exhibit cooperative substrate binding between these subunits.
Homotrophic Effect
binding of one substrate molecule to one subunit of an allosteric enzyme enhances the binding of other substrates to other subunits
Heterotrophic Effect
used in feedback inhibition and feed forward activation
Allosteric Feedback Inhibition
Binding of a specific compound to the allosteric binding site can inhibit the regulatory enzyme of a pathway. The compound is often the end product of a pathway.
Allosteric Feedforward Activation
After a commiting step of a pathway is performed, the last enzyme of a pathway is activated.
Is feedback inhibition performed by a homotrophic effector?
No, by a heterotrophic effector.
Does fructose-1,6-bisphosphate allosterically activate or inhibit pyruvate kinase?
Fructose-1,6-bisphosphate is formed by phosphofructokinase, and is the committed step of glycolysis. This feed-forward activates the enzyme Pyruvate Kinase.
Discuss enzyme induction by insulin.
Insulin signals high blood glucose levels and induces the liver to perform protein synthesis for key enzymes, to perform fatty acid synthesis, and to perform cholesterol synthesis.
Discuss enzyme induction by glucagon.
Glucagon signals low blood glucose levels and induces in the liver key enzymes for gluconeogenesis.
Discuss phosphorylation / dephosphorylation as methods of covalent enzyme modification?
phosphorylation typically inaxctivates an enzyme, while DEphophorylation activates enzymes.
Do Protein Kinases and Phosphatases catalize irreversible reactions? Is the regulation reversible?
The enzymes do indeed catalize irreversible reactions in that a kinase can only add a phosphate, but cannot remove it. A phosphotase must remove the phosphate group. The regulation, however, is reversible, because a phosphate group can be easily removed and the original form can be restored.
Does Insulin or Glucagon lead mainly to phosphorylated key enzymes?
Which hormone induces HMG-CoA Reductase?
Why would high AMP levels lead to phosphorylation of HMG-CoA Reductase. Compare to cAMP system.
HMG-CoA Reductase is activated by substrate availability. After big, carb heavy meals, the enzyme is active. However, high AMP Levels suggest low ATP (cellular energy) levels. In this case, the enzyme is phosphorylated and inactivated.
What is the message signaled to the liver by glucagon?
Glucagon signals to the liver to begin gluconeogenesis and to stop fatty acid and cholesterol synthesis.
How does glucagon perform hormonal regulation of HMG-CoA Reductase?
Glucagon signals via its secondary messenger system to the liver to begin gluconeogenesis and to stop fatty acid and cholesterol synthesis. It also leads to the phosphorylation of HMG-CoA Reductase, thus inactivating it.
Which cells have glucagon receptors? Where are these cells located?
I don't fucking know!
Name two actions of cholesterol on HMG-CoA Reductase?
1. Inhibits transcription of HMG-CoA Reductase
2. Leads to accelerated degradation of HMG-CoA Reductase.