Quiz 07 Results
Question 1: Multiple Choice
Average Score 0.47059 points
Which one of the following stimulates both insulin and glucagon
... [Show More] secretion?
Correct Percent Answered
hyperglycemia 1.176%
somatostatin 1.176%
cortisol 2.353%
hypoglycemia 1.176%
a high protein meal 94.118%
Question 2: Multiple Choice
Average Score 0.42941 points
While volunteering with a medical relief mission in Africa, a college student sampled some local food of
dubious origin, and came down with a bad case of diarrhea. Unable to eat for 3 days, his metabolism
switched to using energy sources other than carbohydrates. Which of the following would you not expect
to happen?
Correct Percent Answered
ketosis 0%
lipolysis 0%
alkalosis 85.882%
glycogenolysis 7.059%
gluconeogenesis 3.529%
uremia (high levels of urea in blood) 3.529%
Question 3: Essay
The attached figure (Glucose Tolerance Graph.jpg) shows results of glucose tolerance tests for 3 male
patients. Glucose tolerance tests involve measuring plasma [glucose] following oral consumption of a
glucose-rich solution. Immediately before drinking the sugar solution, the patients had fasted for several
hours. Normal fasting plasma glucose is about 80 mg/dL. One of the patients is normal, one has diabetes
type 1, and one has chronic liver disease. Identify which patient (A, B or C) is normal, which as diabetes
type 1, and which has chronic liver disease. Briefly explain and justify each of your choices.
Given Answers
Patient C is normal. Patient A has a chronic liver disease. Patient B has diabetes type 1. Patient B is
glucose intolerant because the glucose concentration increases substantially and then maintains a high
level of glucose hours following intake of the glucose solution suggesting that the patient has defective
insulin function thus there is not effective glucose uptake in the body. Patient A maintains a fairly high
glucose concentration following ingestion of the glucose solution. This suggests, that there is some
deficiency in the glucose uptake. Since the liver has the largest stores of glycogen in the body, we can
assume that the liver has a deficiency in glyocogenesis which contributes to Patient B's high plasma
glucose levels hours after ingesting glucose solution. However, since patient A most likely has functioning
inuslin, there are other methods for glucose uptake stimulated by insulin such as insulin mediated glucose
uptake in adipocytes and resting skeletal muscles. Thus, patient A has slightly lower plasma glucose values
compared to Patient B.
2
Patient C appears to have normal glycemia. His fasting glucose is around 80 mg/dL, which is the value. In
addition, patient C's glucose returns to the normal range after the glucose load, indicating that he is body
is able to manage glycemia appropriately.
Patient A appears to have type 1 diabetes. His fasting plasma glucose is abnormally high, which is a sign
that he may be insulin deficient and therefore cannot keep his resting glucose lower. In addition,
administration of glucose causes his glycemia to rise to very high levels, followed by a lack of return to
normal glucose levels. His glycemia remains at around 200mg/dL after the glucose load, indicating that his
body has decreased insulin functioning, which would normally restore glucose levels back to ~80 mg/dL.
By process of elimination, Patient B appears to have chronic liver disease. Patient B's fasting plasma
glucose is abnormally low. This may be caused by chronic liver disease impairing the ability to break down
glycogen into glucose during times of fasting. Normally in a fasted state, the liver will breakdown glycogen
stores in response to low blood glucose to maintain homeostasis.; in the fasted state, the liver will also
use protein stores to perform gluconeogenesis. In chronic liver disease, the ability to store glycogen is
impaired, and the ability to catalyze glycogenolysis is impaired as well; similarly, the liver's ability to make
glucose via gluconeogenesis may be dysfunctional in liver disease. After the glucose is administered,
patient B's plasma glucose increases dramatically and stays high. This may be explained again by the
liver's inability to safely convert glucose into glycogen (glycogenesis) due to chronic liver disease. Chronic
liver disease may also damage hepatocyte sensitivity to insulin or disrupt the signaling cascade present in
hepatocytes. Normally, in the fed state, insulin will bind receptors on hepatocytes and trigger a signal
cascade leading the the activity of hexokinase. Hexokinase phosphorylates glucose into glucose 6
phosphate, effectively keeping intracellular glucose low, maintaining the glucose concentration gradient.
Under normal conditions, this gradient will favor glucose entering the hepatocytes from the plasma,
reducing plasma glucose concentrations. In chronic liver disease, this mechanism of keeping plasma
glucose low may be disrupted, which explains why patient B retains high glycemia after consuming the
glucose load. [Show Less]