Pages 623- 638
What are the three sources of amino acids that are oxidized? What is guano and where does it come from. What is the major chemical component of guano?
Figure 18-1 shows an overview of amino acid metabolism. Where do the carbons end up. Why
is amino acid metabolism different from carbohydrate and lipid metabolism. What do amino
acids have that carbohydrates and lipids do not.
Why is ammonia toxic? (This is not covered in this part of the text--is it covered in
other parts of the text? What about the internet?)
Because ammonia is toxic, excess nitrogen in the body must be excreted or recylced into
other amino acids. What is/are the prinicple carrier(s) of nitrogen in the blood?
You have already learned about the digestive enzymes that breakdown proteins. Pages 626-627 is a review. You need to know where all of these enzymes are made, where and why (what triggers their secretion) they are secreted and what bonds they cleave.
What does pancreatic trypsin inhibitor do? What is acute pancreatitis?
What foods are good sources of vitamin B6? What sort of linkage does PLP form with the amino group of a lysine on the enzyme? What sort of linkage does PLP form with the a carbon of an amino acid. How are aminotransferases named? Be able to draw the structures of the reactants and products for the reaction catalyzed by alanine-a ketoglutarate amino transferase.
What enzymes are used as indicators of heart tissue damage?
In the liver, glutamate is converted to a ketoglutarate and free ammonia. What enzyme catalyzes this reaction, what cofactors are required and what inhibits and stimulates this enzyme?
How is glutamine synthesized in extra-hepatic tissues? What role does glutamine serve in the body? What happens to glutamine in the liver?
The Cori cycle is shown on page 633, figure 18-8 and again on page 875, figure 23-6. The Cori cycle is the conversion of glucose to lactate in anerobic muscle tissue (why does this reaction occur?), the lactate goes through the blood to the liver and in the liver, the lactate is converted to glucose. The glucose is released from the liver and goes through the blood to the tissue.
The Glucose-Alanine cycle is NOT shown on page 633 in figure 18-8. We will have to draw our own figure, based upon the text. In anerobic muscle tissue, pyruvate is either converted to lactate, or it is transaminated. Pyruvate can accept an amino group from other amino acids and then those resulting a keto acids can be used for fuel in the tissue.
Draw the reactants and products for the reaction catalyzed by glutamate-pyruvate transaminase.
The resulting aminated product then leaves the muscle tissue and travels to the liver via the bloodstream. In the liver, the aminated product donates its amino group to glutamate.
Draw the reactants and products for the reaction catalyzed by alanine-aketoglutarate transaminase.
Combine the Cori and Alanine cycles into one picture. (This would make a great quiz question...)
We are ureotelic organisms. (What does that mean? What would we be if we excreted uric acid?) What kind of organisms are bony fishes? You need to know all of the reactions: enzymes, reactants, cofactors, products etc for the urea cycle.
How is the Kreb's cycle connected to the urea cycle.
How is the urea cycle activity increased during starvation or for animals on a high protein diet? (Would you expect this to occur in a diabetic patient? why or why not?)
How is the cycle controlled allosterically? Why is this an enigma?
What is the energy cost for the conversion of two molecules of ammonia to urea?
We must get 10 amino acids from dietary sources as our bodies cannot synthesize them. Defects in the urea cycle require that the patients have very controlled diets--any excess amino acids will be very toxic. Examples of defects and treatments are discussed on pages 637-638.