Metabolism
Biochemistry - Metabolism
Enzyme Function and Activation Energy
(Chapter 6 - Enzyme function and activation energy, n.d.)
Induced Fit Model
(Hudon-Miller, Enzymes, 2013)
Why Does Aldolase B Deficiency Lead to HFI?
• Understanding what happens to Glucose and Fructose in the liver is the first step.
• Glucose enters the liver cell and Glucokinase is in the cytoplasm and adds a Phosphate (Pi) to make G-6-P to keep the glucose in the liver cell, which then becomes G-1-P and can be stored as glycogen or move onto the Citric Acid Cycle (CAC) to make ATP or fatty acids.
• Fructose enters the liver, fructokinase adds a Pi to make F-1-P (the substrate of Aldolase B) to form Aldolase B forming the products DHAP and glyceraldehyde which can then go to glycolysis or onto the (CAC) to make ATP or fatty acids.
• The Lock and Key Model (slide 3) and the Activation Engery Ea (slide 2) will help to explain how
Aldolase B is the catalyst to convert F-1-P in the liver.
• The Lock and Key Model shows how an enzyme and substrate attach, the enzyme then converts the substrate to the product and then releases the product. One of the important factors is that the enzyme then continues on without being changed.
• The Ea shows how the substrate on its own requires a certain amount of free energy but with an enzyme the amount of free energy in the Ea is decreased. The enzyme is the catalyst that works to lower the Ea without being used in the reaction. Again the enzyme is unchanged during this process. Why Does Aldolase B Deficiency Lead to HFI?
• When Blood Sugar (BS) is high:
• Glucokinase is in the cytoplasm. Glycogen is stored. Glucose moves through glycolysis and CAC to make ATP and Fatty Acids.
• F-1-P acts like a signal for the Glucokinase to come out of the nucleus and into the cytoplasm.
• When BS is low:
• Glycogen is broken down, the Pi is taken off and can then be released into the blood to stabilize the BS.
• F-1-P is low and
Enzyme Function and Activation Energy
(Chapter 6 - Enzyme function and activation energy, n.d.)
Induced Fit Model
(Hudon-Miller, Enzymes, 2013)
Why Does Aldolase B Deficiency Lead to HFI?
• Understanding what happens to Glucose and Fructose in the liver is the first step.
• Glucose enters the liver cell and Glucokinase is in the cytoplasm and adds a Phosphate (Pi) to make G-6-P to keep the glucose in the liver cell, which then becomes G-1-P and can be stored as glycogen or move onto the Citric Acid Cycle (CAC) to make ATP or fatty acids.
• Fructose enters the liver, fructokinase adds a Pi to make F-1-P (the substrate of Aldolase B) to form Aldolase B forming the products DHAP and glyceraldehyde which can then go to glycolysis or onto the (CAC) to make ATP or fatty acids.
• The Lock and Key Model (slide 3) and the Activation Engery Ea (slide 2) will help to explain how
Aldolase B is the catalyst to convert F-1-P in the liver.
• The Lock and Key Model shows how an enzyme and substrate attach, the enzyme then converts the substrate to the product and then releases the product. One of the important factors is that the enzyme then continues on without being changed.
• The Ea shows how the substrate on its own requires a certain amount of free energy but with an enzyme the amount of free energy in the Ea is decreased. The enzyme is the catalyst that works to lower the Ea without being used in the reaction. Again the enzyme is unchanged during this process. Why Does Aldolase B Deficiency Lead to HFI?
• When Blood Sugar (BS) is high:
• Glucokinase is in the cytoplasm. Glycogen is stored. Glucose moves through glycolysis and CAC to make ATP and Fatty Acids.
• F-1-P acts like a signal for the Glucokinase to come out of the nucleus and into the cytoplasm.
• When BS is low:
• Glycogen is broken down, the Pi is taken off and can then be released into the blood to stabilize the BS.
• F-1-P is low and