Final Exam Study Guide
- Explain the various clinical findings in
detailed biochemical terms, as requested below.
- 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.
- 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.
- Why do both fructose and glycerol produce
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.
- 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
- 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.
- Why is she getting fat deposition in her
- 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.
- Why is she so subject to acidosis?
- 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.
- 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
Last modified 3 May 2011