CLINICAL CASES
195
[21.3]
A known alcoholic is found lying semiconscious at the bottom of a
stairwell with a broken arm by his landlady, who called an ambulance
to take him to the emergency room. Initial laboratory studies showed a
relatively large anion gap of 34 (normal = 9 to 15). His blood alcohol
was elevated at 245 mg/dL (intoxication level = 150 to 300 mg/dL),
and his blood glucose was 38 mg/dL (low normal). The patient’s large
anion gap and hypoglycemia can best be explained by which of the
following?
A. Decreased secretion of glucagon
B. Increased secretion of insulin
C. Increased urination resulting from the diuretic effect of alcohol
D. Inhibition of dehydrogenase enzymes by NADH
E. Inhibition of glycogenolysis by ethanol
A nsw ers
[21.1]
D. At the beginning of the race, a runner running at a reasonable pace
consumes energy at a ratio of approximately 75 percent carbohydrate:
25 percent fatty acids. However, by the end of the race, glycogen
stores are for the most part depleted, and the generation of ATP must
come from the P-oxidation of fatty acids, which produces reducing
equivalents for oxidative phosphorylation. This requires an increase
in the amount of oxygen consumed.
[21.2]
C. The activity of regulatory enzymes such as fructose-1,6-bisphos-
phatase, hexokinase, phosphofructokinase 1, and pyruvate kinase are
frequently controlled by binding allosteric effectors. These allosteric
enzymes usually exhibit sigmoidal kinetics. Lactate dehydrogenase is
not controlled by allosteric effectors and therefore would be expected
to exhibit Michaelis-Menten kinetics.
[21.3]
D. Alcoholics frequently do not eat while binge drinking, so it is most
likely that his liver glycogen stores became depleted and could not
increase his blood glucose levels. The metabolic stress leads to the
increase in secretion of epinephrine and other hormones that mobilize
fatty acids from stored triglycerides in adipose cells. These fatty acids
undergo P-oxidation in the liver but are converted to ketone bodies
because of the inhibition of the TCA cycle by high levels of NADH
produced by the oxidation of ethanol first to acetaldehyde and
acetate. Key gluconeogenic dehydrogenases are also inhibited by the
elevated levels of NADH, including lactate dehydrogenase, glycerol
3-phosphate dehydrogenase, and malate dehydrogenase.
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