Humboldt State University ® Department of Chemistry

Richard A. Paselk

Chemistry 438 - Spring 2011

 Final Exam Study Guide


Explain the various clinical findings in detailed biochemical terms, as requested below.
  1. Why is the patient so liable to hypoglycemia? She cannot convert anything below F-1,6-bisP to glucose. Thus once her supply of liver glycogen is used up, she cannot use gluconeogenesis to make glucose.
    1. Does glucose result in hypoglycemia? Glucose itself does not result in hypoglycemia since it can be used or stored as glycogen, which may then release glucose to the blood stream.
    2. Why do both fructose and glycerol produce hypoglycemia? Fructose and glycerol both enter liver glycolysis below F-1,6-bisP and therefore cannot be used to make glucose. Ingesting either will therefore not provide any glucose, nor will they replenish glycogen, leading to a fall-off of glucose and hypoglycemia.
  2. Would you expect amino acid metabolism to be affected by her condition (does does her condition mimic fasting, overeating, or normal feeding - think)? Yes, it will affect amino acid metabolism since it mimics fasting in the sense that here glucose levels fall inducing her body to try to replace the glucose via gluconeogenesis from amino acids.
    1. How and why? Since her serum glucose levels fall precipitously, she will breakdown muscle protein to provide amino acids to the liver for gluconeogenesis. Unfortunately she can't use the amino acids for gluconeogenesis, so she continues to breakdown protein. She will also be using alanine and glutamine to help transport nitrogen from the branched chain amino acids metabolized in the liver in this process.
  3. Why is she getting fat deposition in her liver?
    1. What is/are the metabolic source/s? (Give a thorough, "all encompassing" picture of sources and reasoning.) The continuing signal that she is "starving" means that adipose tissue will be sending fatty acids to the liver for conversion to ketone bodies. But the liver is also getting amino acids for gluconeogenesis, which it cannot use. They must thus go to AcCoA and ketone bodies or fat. When fructose or glycerol are consumed, they also must be converted to fat. Thus the liver is simply overwhelmed with fat inputs and ends up forming fat deposits.
  4. Why is she so subject to acidosis?
    1. What compounds would you expect are contributing to the acidosis? From above we expect significant concentrations of ketone bodies. Amino acids and sugars will also contribute pyruvate (the high fat and AcCoA concentrations will inhibit Pyruvate DH Complex) which in turn can form lactate - all of which are acidic.
    2. Why the change in carbon dioxide concentration? Two effects may be at work. 1) Simply lowering the pH will tend to lower the carbon dioxide concentration as a simple equilibrium effect (bicarbonate + a proton gives carbon dioxide and water). 2) Physiologically, acidosis induces "panting" which results in "blowing off" carbon dioxide in the lungs since the carbon dioxide concentration in lungs and blood are greater than atmospheric concentrations.


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Last modified 3 May 2011